Botanically, Althaea officinalis is a perennial herb native to Western Asia and Europe, favoring humid soils, with stems that can reach 1.5 meters in height and diameters of up to 5 centimeters. Today it is cultivated worldwide not only for medicine but also for food and dietary supplements, and its vivid flowers make it a popular ornamental. Its roots and leaves appear in teas and salads and are valued for sedative and emollient qualities, while pharmaceutical raw materials are drawn from the roots and leaves. Historically, the root has been applied to skin burns, insect bites, catarrh, ulcers, abscesses, constipation, diarrhea, dry cough, mild gastritis, and irritation of the mouth and throat mucosa.

The chemical analysis is where the review becomes particularly striking. Researchers have isolated and identified 46 distinct compounds from various parts of the plant, with flavonoids dominating the list at 17 specific molecules, including quercetin, kaempferol, hypolaetin glycosides, and astragalin. The roots have yielded three coumarins, and steroids and triterpenoids such as beta-sitosterol and lanosterol have been isolated from roots and seeds. Perhaps most significant are the polysaccharides: the mucilage content varies between 5 and 11.6 percent depending on seasonal growth conditions and includes acidic arabinogalactans, galacturonic rhamnans, arabans, and glucans. Phenolic acids such as caffeic, ferulic, chlorogenic, vanillic, and salicylic acid round out the profile. The authors caution that the chemical makeup shifts with cultivar, flower and leaf color, climate, drying method, and storage conditions, a variability that complicates standardization but helps explain inconsistent results across studies.

Antioxidant activity has been tested extensively, with instructive nuances. In one study, water extracts of the root showed no antioxidative activity, whereas ethanol-water mixtures performed well, and lower ethanol concentrations (50:50 and 70:30) outperformed higher ones in scavenging ABTS radicals and hypochlorite ions, correlating with higher phenolic and flavonoid content. Polysaccharides isolated from the plant showed dose-dependent DPPH radical scavenging between 0.25 and 4 milligrams per milliliter, though their IC50 of 1.53 milligrams per milliliter was higher, meaning less potent, than vitamin C. Other work found polysaccharides stabilizing 28 to 57 percent of DPPH compounds in the 1.0 to 5.0 milligram per milliliter range. Notably, a petroleum ether fraction achieved 94.8 percent hydroxyl radical scavenging at 20 milligrams per milliliter, exceeding ascorbic acid’s 81.6 percent at the same concentration, an effect attributed to the uronic acid content of the root. Optimized extraction conditions, including a temperature of 55.51 degrees Celsius and a 12.11-hour duration, pushed polysaccharide antioxidant activity to 84.94 percent, although prolonged extraction and elevated temperatures degraded activity.

The antibacterial evidence spans both Gram-positive and Gram-negative organisms. A methanol extract inhibited Klebsiella aerogenes, Streptococcus pneumoniae, Staphylococcus aureus, and Pseudomonas aeruginosa, with minimum inhibitory concentrations of 50 to 100 milligrams per milliliter. Against antibiotic-resistant Staphylococcus aureus strains isolated from patients, an ethanolic extract showed MIC and MBC values of 3.2 and 6.5 milligrams per milliliter. In one of the more remarkable findings, a methanol extract outperformed the antibiotic gentamicin against Klebsiella pneumoniae across all tested concentrations, with inhibition zones reaching 21.2 millimeters, and matched ciprofloxacin’s effectiveness against Escherichia coli, Klebsiella pneumoniae, and Shigella dysenteriae. The authors of that study uniquely identified triterpenoids such as lanosterol and fatty acids as the active antibacterial components, noting that chain length determines the spectrum: shorter chains inhibit Gram-negative bacteria, longer chains Gram-positive species, and chains of 10 to 12 carbons inhibit yeasts.

The mechanisms behind these effects are multifaceted. Flavonoids inhibit nucleic acid synthesis, disrupt cytoplasmic membranes, interfere with energy metabolism, prevent bacterial adhesion, and block biofilm formation. Phenolic compounds modify membrane permeability by accumulating hydrophobic groups in the phospholipid bilayer and bind essential enzymes involved in protein, DNA, and RNA synthesis. Against Gram-positive bacteria specifically, the extract appears to adhere to N-acetylglucosamine in the bacterial cell wall, and polyphenols may generate hydrogen peroxide that suppresses bacterial growth. However, the review also documents limits: hydroethanolic extracts were ineffective against Gram-negative bacteria in some studies, and the extract performed less well than penicillin and 0.2 percent chlorhexidine against Streptococcus mutans and Lactobacillus acidophilus, even though it showed stronger activity against S. mutans than L. acidophilus.

Anti-inflammatory research provides some of the most mechanistically detailed results. In human macrophage models, an ethanol root extract protected cells from hydrogen peroxide-induced cytotoxicity and reactive oxygen species production, and inhibited the release of the inflammatory cytokines TNF-alpha and interleukin-6 to the same degree as diclofenac, without impairing mitochondrial membrane potential. In endothelial cells, the extract reduced interleukin-6 release by up to 24 percent and reactive oxygen species by 16 to 18 percent, while improving wound closure by 10 to 13.5 percent in a six-hour migration assay. The polysaccharides appear to form a protective film on inflamed mucous membranes, and high-molecular-weight hyaluronic acid in the extract may stimulate leukocyte movement and epithelial growth factors, promoting tissue regeneration. In a rat model of chemically induced liver damage, the extract alone improved cytokine levels without statistical significance, but combined with the standard hepatoprotective drug silymarin it significantly reduced all pro-inflammatory cytokines and raised interleukin-10, apparently modulating the Bax/Bcl-2/p53 and PI3K/Akt/mTOR signaling pathways.

Wound-healing studies reinforce the plant’s traditional use. A polyherbal ointment combining Althaea officinalis with Rosa damascena and Lavandula angustifolia essential oils achieved a healing percentage of 99.07 in grade III skin wounds, with histology confirming complete re-epithelialization, healthy granulation tissue, enhanced angiogenesis, and reduced scarring. In rats, a water-ethanol gel significantly increased collagen volume density and fibroblast populations, effects linked to N-phenylpropenoyl-L-amino acids that stimulate keratinocytes. A 15 percent ointment of the flower mucilage shortened healing time with no adverse effects, performing comparably to phenytoin ointment. The mucilage components, pectin, tannin, and polysaccharides, each contribute: tannic acid promotes angiogenesis and raises vascular endothelial growth factor, pectin maintains wound moisture and oxygen availability, and polysaccharides support new epithelial cell formation.

The antitussive evidence is the most clinically advanced. In a trial of 822 patients with dry cough and throat irritation, both lozenge and syrup forms of an aqueous root extract provided relief within 10 minutes, with only three minor adverse events. Among 63 patients with cough induced by angiotensin-converting enzyme inhibitor drugs, cough severity scores fell from 2.66 to 1.23 with the extract versus 2.7 to 2.33 with placebo, though lung function measures were unchanged. A post-marketing study of 313 children aged 0 to 12 reported high effectiveness in 84.3 percent of cases and 97 percent tolerability, while a retrospective study of 599 children found positive results in 90 percent of cases with no adverse effects. In comparative trials, a herbal solution containing Althaea officinalis and Zataria multiflora improved cough symptoms by 65.5 percent versus 39.4 percent for dextromethorphan.

Safety data are broadly reassuring. Hemolytic activity testing showed a hemolysis rate of just 2.6 percent, the acute oral toxicity in mice exceeded 5,000 milligrams per kilogram, and the plant is considered safe during pregnancy and lactation, though it may delay absorption of other medications. The review’s authors conclude that while the existing evidence supports the therapeutic applications of Althaea officinalis, further clinical trials using disease models are necessary to fully establish its ethnopharmacological profile. For a plant that has straddled the boundary between kitchen and pharmacy for millennia, the message is clear: its mucilage, flavonoids, and phenolic acids are not folklore but measurable pharmacology, now awaiting the rigorous clinical validation that modern medicine demands.

Subject of Research: Phytochemistry and pharmacological activities of the medicinal plant Althaea officinalis

Article Title: Pharmacological effects and phytochemical profile of Althaea officinalis

Article References: Sadanov, A., Baimakhanova, G., Orasymbet, S., Ratnikova, I., Baimakhanova, B., Smirnova, I., Kantureyeva, A., Zhakipbekov, K., Tolenova, K., & Turgumbayeva, A. (2026). Pharmacological effects and phytochemical profile of Althaea officinalis. Pharmacia, 73, Article e196211. https://doi.org/10.3897/pharmacia.73.e196211

Image Credits: AI Generated

DOI: 10.3897/pharmacia.73.e196211

Keywords: Althaea officinalis, marshmallow root, phytochemistry, flavonoids, polysaccharides, antitussive, anti-inflammatory, antioxidant, antibacterial, wound healing, herbal medicine, mucilage

The choice of the azoxymethane/dextran sulphate sodium model is significant for interpreting these findings. This two-step protocol first exposes mice to a genotoxic carcinogen and then subjects them to repeated cycles of colonic epithelial injury and repair, producing tumours that arise on a background of chronic inflammation. That sequence mirrors one of the recognised pathways of human colorectal carcinogenesis, in which persistent inflammatory conditions such as colitis precede and promote malignant transformation. Because inflammation is not merely a by-product but an active driver in this model, interventions that dampen inflammatory signalling can be evaluated for their potential to interrupt the tumour-promoting feed-forward loop between tissue damage, immune activation, and epithelial proliferation.

Interleukin-6 occupies a central position in this loop. Produced by epithelial cells, macrophages, and other immune populations in the gut, it activates signalling pathways that promote epithelial cell survival, proliferation, and resistance to apoptosis, thereby creating conditions favourable for tumour expansion. The observation that menaquinone-7 supplementation and supplementation with the vitamin K2-producing Lactobacillus plantarum strain both reduced interleukin-6 levels therefore points to a plausible mechanistic target. The concurrent improvement in the localisation of interleukin-10, an anti-inflammatory cytokine, suggests a rebalancing of the mucosal immune environment rather than simple global immunosuppression, which would be an undesirable outcome in a cancer context.

The elevated interleukin-10 seen in untreated AOM/DSS-control mice deserves particular attention. Although interleukin-10 is generally regarded as protective and anti-inflammatory, tumours can co-opt immunosuppressive cytokine networks to build a microenvironment that shields malignant cells from effective immune surveillance. The pattern observed in the control animals, with elevated interleukin-10 accompanying chronic mucosal inflammation and glandular distortion, is consistent with the establishment of such an immunosuppressive tumour microenvironment. The shift toward more homeostatic interleukin-10 distribution in the treated groups may therefore reflect a normalisation of immune regulation rather than a simple increase or decrease in any single cytokine.

The nuclear factor kappa B pathway provides a candidate molecular link between the vitamin K2 interventions and the cytokine changes measured in the study. This transcription factor family sits upstream of many inflammatory genes, including those encoding interleukin-6, interleukin-8, and tumour necrosis factor alpha, and its constitutive activation is a well-documented feature of inflammation-associated cancers. Inhibition of this pathway can therefore cascade into coordinated reductions across multiple pro-inflammatory mediators, which is the pattern the authors observed across all vitamin K2 interventions. Confirming this mechanism definitively in vivo would require additional experimentation, but the consistency of the cytokine modulation across homologues with very different absorption profiles lends indirect support to a pathway-level effect.

The microbiological dimension of the study adds a layer of complexity that distinguishes it from simple nutraceutical experiments. By combining next-generation sequencing with classical culture methods, the researchers could track both the overall composition of the gut community and the abundance of specific Lactobacillus species. The finding that menaquinone-9 supplementation markedly increased faecal Lactobacillus abundance despite its poor absorption raises the possibility that this long-chain homologue acts partly as a substrate or selective factor favouring lactobacilli in the lumen. If so, the anti-inflammatory activity of menaquinone-9 could be mediated at least in part through reshaping the microbial community rather than through direct effects on host tissue, an interpretation that would align with the growing recognition that microbiota composition is itself a modifiable determinant of colonic inflammation.

The use of a naturally produced form of vitamin K2, generated by a Lactobacillus plantarum strain rather than supplied as a purified synthetic compound, bridges two research traditions that have largely developed in parallel: probiotic therapy and vitamin-based chemoprevention. Certain intestinal bacteria, lactobacilli among them, are known to synthesise menaquinones, and the study’s design allowed the authors to compare a bacterial source of the vitamin with chemically defined homologues. The comparable anti-inflammatory effects observed with the natural preparation and with menaquinone-7 suggest that the bioactive molecule, rather than the delivery vehicle, drives much of the effect, although the probiotic strain may contribute additional benefits through its own interactions with the mucosal immune system.

Methodologically, the quantification of menaquinones by ultra-pressure liquid chromatography coupled to tandem mass spectrometry with atmospheric pressure chemical ionisation represents an important strength. Vitamin K2 homologues are hydrophobic molecules that differ only subtly in side-chain length, making their separate quantification in complex biological matrices technically demanding. The ability to measure individual homologues in both faeces and colonic homogenates is what made it possible to detect the divergent absorption behaviours of menaquinone-4, -7, and -9, a distinction that would have been invisible if only total vitamin K activity had been assessed. The supplementary detection of menaquinone-5 and menaquinone-6 in these samples further indicates that the analytical method captured intermediate homologues, with menaquinone-5 in the colon falling below the limit of detection in all groups.

The immunofluorescence and western blotting approaches used to profile cytokine expression complement each other in a useful way. Immunofluorescence preserves spatial information, revealing where within the mucosal architecture a given cytokine is being produced, which is essential for interpreting changes in the tumour microenvironment where immune cells, epithelial cells, and stromal components are unevenly distributed. Western blotting provides quantitative protein-level confirmation. Together these methods allowed the authors to describe not just how much of each cytokine was present but how its distribution across the tissue changed with treatment, which is how the improved localisation of interleukin-10 was identified.

It is worth emphasising what the mouse model can and cannot establish. The AOM/DSS protocol reliably reproduces inflammation-driven colonic tumorigenesis and is widely used for preclinical chemoprevention research, but the inflammatory and microbial context of the laboratory mouse differs from that of human patients, whose tumours arise over decades against a backdrop of individual diet, microbiota, and immune history. The BALB/c strain used here is an inbred line, which reduces variability within the experiment but also limits the genetic diversity over which the findings can be generalised. Translating these results into human chemoprevention strategies will require studies that account for human microbiome variability, dietary vitamin K intake, and the pharmacokinetics of menaquinone supplementation in people with existing colonic pathology.

The dosing and formulation details recorded in the supplementary materials, including the composition of the purified diets and the preparation procedures for each homologue, matter for reproducibility and for future comparative work. Because menaquinones are fat-soluble and vary in bioavailability depending on the vehicle and dietary matrix, standardised dietary composition is essential when comparing interventions across laboratories. The documentation of these procedures, together with the semi-quantitative histopathological scoring criteria for mucosal and submucosal damage, provides a framework that other groups can adopt when testing related interventions.

The collaborative structure of the research team reflects the multidisciplinary demands of this kind of study. Microbiologists at Jagiellonian University Medical College handled the bacterial strain characterisation and culture work, veterinary scientists contributed to the animal model, analytical chemists developed the mass spectrometric quantification of menaquinones, oncologists and cancer metabolism researchers contributed expertise on the tumour biology, and pathologists performed the histopathological assessment. This breadth was necessary because the central question, whether a bacterial vitamin can modulate inflammation in a way that alters cancer-relevant biology, spans microbiology, nutrition, immunology, and oncology simultaneously.

Looking forward, several questions follow naturally from these findings. Whether the cytokine modulation observed during the intervention translates into reduced tumour burden or improved survival in longer-term follow-up is a critical next step. Whether the NF-kappa B pathway inhibition is direct or mediated through upstream changes in the microbiota or in epithelial barrier function remains to be resolved. And whether the homologue-specific differences in absorption and microbiota effects persist in animals with more diverse microbial communities, or in humans, will determine which menaquinone, if any, is best suited for chemoprevention trials. The open access publication of this work, funded by the National Science Centre Poland, ensures that these questions can be pursued by any laboratory with the appropriate model systems and analytical capabilities.

Subject of Research: colorectal cancer

Article Title: Anti-inflammatory effects of vitamin K2 and Lactobacillus plantarum in a mouse model of colorectal cancer

Article References: Strus, M., Wójcik, A., Gruszka, A. M., Meyger, Ł., Kuziak, A., Kasperski, T., Arent, Z., Pardyak, L., Dubniewicz, K., Baś, B., Piwowar, P., Żeber-Lubecka, N., Kij, A., Okoń, K., Stanek, M., & Jedlińska, K. (2026). Anti-inflammatory effects of vitamin K2 and Lactobacillus plantarum in a mouse model of colorectal cancer. BMC Biology. https://doi.org/10.1186/s12915-026-02742-0

Image Credits: AI Generated

DOI: 10.1186/s12915-026-02742-0

Keywords: vitamin K2, menaquinones, Lactobacillus plantarum, colorectal cancer, gut microbiota, cytokines, NF-κB, mouse model, probiotics, chemoprevention, Anti-inflammatory, effects

H. pylori is no ordinary stomach dweller. The World Health Organization has classified it as a Group 1 carcinogen since 1994, and colonization of the gastric mucosa by the spiral-shaped, microaerophilic bacterium remains the single major risk factor for gastric cancer. Its persistence hinges on an arsenal of virulence factors, including outer membrane proteins that function as adhesins, molecular grappling hooks that anchor the bacterium to gastric epithelial cells and allow it to resist clearance by mucus turnover, acid flow, and peristalsis. Chief among these adhesins are BabA, which binds Lewis b blood group antigens; SabA, which recognizes sialyl-Lewis X structures; and HopQ, which latches onto members of the CEACAM glycoprotein family. Adhesion is not merely a docking maneuver: successful binding enables the delivery of additional virulence factors such as urease and the cytotoxins CagA and VacA, and it precedes the chronic inflammation that can progress to metaplasia, dysplasia, and carcinoma.

The therapeutic landscape has grown increasingly hostile. Clarithromycin resistance undermined the classic triple therapy of a proton-pump inhibitor plus amoxicillin and clarithromycin, prompting a shift to bismuth-based quadruple regimens built on tetracycline and metronidazole. Yet metronidazole resistance has now been detected at rates that surpass clarithromycin resistance in multiple territories, threatening the fallback regimen as well. Against this backdrop, researchers at the Federal University of Espírito Santo and the Federal University of Santa Catarina in Brazil set out to test whether a standardized silymarin preparation could attack H. pylori on several fronts at once: growth, adhesion, and inflammation.

Silymarin itself is not a single molecule but a mixture of flavonolignans that can constitute up to 70 percent of the crude extract from milk thistle fruits and seeds. The complex is dominated by the enantiomeric pairs silybinin A and B, which together can account for as much as 70 percent of the mixture, alongside isosilybinin A and B, silychristin, isosilychristin, silydianin, and the flavonoid taxifolin. All carry a flavonoid moiety, which underpins the complex’s celebrated antioxidant activity and its long history of use in hepatoprotection, anti-inflammatory, and antifibrotic formulations. Previous work by some of the same team had already shown that silybinin alone inhibits H. pylori, prompting the question of whether the full phytocomplex might perform even better.

The answer, at least in vitro, appears to be yes. Using the broth microdilution method against the reference strain H. pylori ATCC 43504, a strain known to be amoxicillin-susceptible and metronidazole-resistant, the researchers determined a minimum inhibitory concentration of 128 micrograms per milliliter, achieving 90.46 percent growth inhibition. Critically, the minimum bactericidal concentration matched the MIC, meaning the same dose that halted growth also killed the bacteria outright. For comparison, amoxicillin showed an MIC of 0.0625 micrograms per milliliter while metronidazole required 256 micrograms per milliliter against this resistant strain, confirming the expected susceptibility profile.

Scanning electron microscopy then revealed what the treatment does to the bacterium’s architecture. Untreated cells displayed the archetypal helical morphology with smooth surfaces and intact organization. After exposure to half the MIC of silymarin, the bacteria exhibited surface irregularities, cellular deformation, and the emergence of coccoid-like round forms, a pattern consistent with a membrane-targeted mechanism. The changes resembled, though were less extensive than, the severe membrane disruption caused by amoxicillin, which destroys the cell wall. Prior studies suggest silymarin increases membrane permeability, and its flavonolignans have been linked to interference with protein and RNA synthesis as well as disruption of the enzymes bacteria need for energy production.

Safety and selectivity were addressed before any anti-inflammatory claims could be made. In MTT assays, silymarin showed an IC50 of 46.27 micrograms per milliliter against AGS gastric adenocarcinoma cells and 98.18 micrograms per milliliter against RAW 264.7 macrophages, yielding a selectivity index of 2.12, roughly a twofold preference for killing cancer cells over healthy immune cells. Cisplatin, by contrast, showed almost no selectivity between the two cell types. Importantly, at the concentrations used in the immunological experiments, macrophage viability remained above 90 percent, ensuring that the dramatic reductions in inflammatory mediators were genuine pharmacological effects rather than artifacts of cell death.

Those effects were substantial. When macrophages were stimulated with H. pylori and treated with 50 micrograms per milliliter of silymarin, production of tumor necrosis factor-alpha fell by 80.82 percent, interleukin-6 dropped by 76.24 percent, and nitric oxide plummeted by 97.50 percent. Each mediator matters: TNF-alpha activates the NF-kappaB pathway that amplifies the inflammatory cascade and has been implicated in gastric carcinogenesis, while IL-6 drives a feedback loop between macrophages and gastric epithelial cells that promotes cancer, and sustained nitric oxide generates reactive nitrogen species capable of oxidative DNA damage. Notably, the complex outperformed pure silybinin on nitric oxide suppression, 97.50 percent versus 73.33 percent in earlier work, hinting at additive or synergistic contributions from the full flavonolignan mixture.

Adhesion assays added a third dimension to the picture. Using fluorescence-labeled H. pylori and AGS gastric cells, the team found that silymarin inhibited bacterial attachment in a concentration-dependent manner, with the highest tested dose of 256 micrograms per milliliter reducing adhesion by 25.87 percent. That figure is moderate, but it sits within the range reported for other natural anti-adhesive agents, including green tea epigallocatechin gallate, cranberry proanthocyanidins, and garlic-derived organosulfur compounds. Because attachment is the critical first step in colonization, even partial interference could impair the establishment of infection, and blocking adhesin binding sites may also indirectly dampen the expression of virulence factors such as VacA and CagA.

To probe the mechanism, the researchers turned to molecular docking, individually fitting all eight major silymarin constituents into the crystal structures of BabA, SabA, and HopQ. Isosilybinin A scored highest against BabA, forming hydrogen bonds with residues CYS189 and SER244; isosilychristin performed best against SabA, interacting with LYS152 and GLN159; and silychristin led against HopQ through contacts with SER135, ILE130, and ILE242. The results were validated with a consensus docking strategy using AutoDock Vina, since no co-crystallized small-molecule inhibitors exist for these adhesins. Encouragingly, the key residues targeted are highly conserved across H. pylori strains, and their substitution is known to cripple adhesin function. The authors caution that docking was performed on isolated compounds rather than the whole extract, so the computational results support plausible ligand-target interactions but do not fully explain the activity of the intact phytocomplex.

Physicochemical predictions rounded out the evaluation. All eight compounds showed mildly lipophilic logP values between 0.85 and 1.85 with satisfactory aqueous solubility, and all complied with Lipinski’s rule of five, the classical benchmark for oral drug-likeness. That profile is consistent with silymarin’s decades of oral use as a phytotherapeutic agent. Taken together, the study positions the milk thistle complex as a genuinely multifunctional candidate against H. pylori, one that simultaneously curbs bacterial growth, disrupts cellular architecture, suppresses three major inflammatory mediators, and undermines the adhesion machinery the pathogen depends on. The work remains at the in vitro and computational stage, and clinical translation will require further validation, but it offers a compelling case that an ancient herbal remedy may hold modern answers to one of medicine’s most stubborn gastric adversaries.

Subject of Research: Antibacterial, anti-inflammatory, and anti-adhesive effects of silymarin from milk thistle against Helicobacter pylori

Article Title: Effect of silymarin on Helicobacter pylori growth and adhesion: in vitro and in silico evaluation

Article References: Majeski, V. Z., Bittencourt, M. L. F., Tregnago, P. H., Loose, D. N., Federico, L. B., Kitagawa, R. R., & Ribeiro Gonçalves, R. D. C. (2026). Effect of silymarin on Helicobacter pylori growth and adhesion: in vitro and in silico evaluation. Frontiers in Natural Products, 5, Article 1890760. https://doi.org/10.3389/fntpr.2026.1890760

Image Credits: AI Generated

DOI: 10.3389/fntpr.2026.1890760

Keywords: silymarin, Helicobacter pylori, milk thistle, flavonolignans, antibacterial, anti-inflammatory, molecular docking, adhesins, gastric cancer, natural products, antibiotic resistance, Silybum marianum

The study examined 28 patients with confirmed SARS-CoV-2 infection who also had active surgical conditions, treated between 2020 and 2022. Most were elderly—mean age 63.5 years, with ages ranging from 28 to 101—and 22 carried an underlying malignancy. Twenty-two underwent surgery during their hospital stay, with procedures classified as major in nearly 43 percent and very major in another 32 percent. COVID-19 was diagnosed after surgery in more than two-thirds of cases, before surgery in four patients, and during preoperative evaluation in five who never reached the operating table.

Thirteen patients received a high-dose colchicine protocol: 4 milligrams daily for the first two days, tapering to 3 milligrams on day three, 2.5 on day four, 2 on days five and six, and 1.5 daily thereafter for up to 28 days. This regimen was previously described in a remarkable case report involving a 101-year-old man who developed COVID-19 after two major emergency abdominal operations and recovered fully on the same protocol. Treatment allocation was not randomized—most patients who did not receive colchicine were treated before the drug entered local practice, while others had contraindications or could not take oral medication.

The laboratory findings are perhaps the most biologically compelling aspect of the study. Serum ferritin, a protein intimately linked to macrophage activation and NLRP3 inflammasome-driven inflammation, was dramatically lower in the colchicine group: 401.3 micrograms per liter compared to 1,592.3 in untreated patients, a difference that reached statistical significance. C-reactive protein and D-dimer, while not reaching conventional significance thresholds, both trended lower in treated patients. This concordant pattern across three biomarkers of inflammation and coagulation suggests a coherent biological signal consistent with colchicine’s proposed mechanism of action.

Colchicine works by disrupting microtubule polymerization, thereby dampening neutrophil activation and migration, and indirectly inhibiting the NLRP3 inflammasome—a multiprotein complex that, when activated, triggers the release of interleukin-1β and interleukin-6, driving the cytokine storm characteristic of severe COVID-19. The idea is that if you can intervene before this inflammatory cascade becomes fully established, you might prevent the downstream tissue damage that kills patients. Ferritin, being particularly reflective of macrophage activation, is exactly the biomarker you would expect to fall if this mechanism were operating.

Clinical outcomes, while statistically inconclusive, were striking in their direction. Only one of thirteen colchicine-treated patients died in hospital (7.7 percent), compared to six of fifteen untreated patients (40 percent). The unadjusted relative risk of 0.19 did not reach conventional significance, with a confidence interval spanning from 0.03 to 1.40. Similarly, at least one documented postoperative or systemic complication—ranging from respiratory failure and sepsis to wound dehiscence and relaparotomy—occurred in 30.8 percent of treated patients versus 46.7 percent of untreated patients. These differences are hypothesis-generating at best, but their magnitude and consistency with the biomarker data warrant attention.

The broader context matters here. The prevailing clinical consensus that colchicine offers little benefit in COVID-19 rests heavily on the RECOVERY trial, which enrolled roughly 40 percent of all participants in pooled randomized analyses of the drug. RECOVERY tested low-dose colchicine initiated late in hospitalized patients with established disease. But an increasing body of evidence suggests that timing and dose are critical variables. A 2026 randomized, double-blind trial administering 2 milligrams daily for five days (cumulative dose of 10 milligrams) to critically ill, mechanically ventilated COVID-19 patients found results consistent with the potential benefit of higher cumulative doses. Several observational studies and clinical reports have similarly reported favorable outcomes with earlier initiation and higher loading doses.

The surgical population presents a uniquely vulnerable setting for COVID-19. Major operations induce systemic inflammation, transient immune dysfunction, endothelial activation, and a prothrombotic state. Superimpose SARS-CoV-2 infection—with its pulmonary injury, dysregulated inflammation, and microvascular thrombosis—and the physiological reserve needed to recover from surgery can be overwhelmed. The COVIDSurg Collaborative reported a 30-day mortality of 23.8 percent in perioperative COVID-19 patients, with pulmonary complications in roughly half. The mortality observed in the current cohort—25 percent overall—falls squarely within this range, underscoring the severity of this clinical scenario.

Timing of infection relative to surgery emerged as another critical variable. Postoperative COVID-19 diagnosis was associated with worse outcomes in recent studies of gastrointestinal surgery patients, and the COVIDSurg/GlobalSurg cohort found that mortality remained elevated when surgery occurred within six weeks of infection, approaching baseline only after a seven-week delay. Yet postponing surgery carries its own risks: modeling by Sud and colleagues suggested that even modest delays in cancer surgery could negatively affect survival, with the magnitude varying by tumor type and stage. One patient in the current cohort experienced documented progression of malignancy following delayed adjuvant treatment—a sobering illustration of the competing risks clinicians must navigate.

The study’s limitations are substantial and acknowledged by its authors. With only 28 patients and seven deaths, statistical power was minimal, confidence intervals were wide, and multivariable adjustment was impossible. Treatment allocation was confounded by calendar time, as most untreated patients were hospitalized during an earlier pandemic period when viral variants, population immunity, and supportive care differed. Ferritin measurements were available for only 17 patients. Some patients could not receive colchicine precisely because they were too ill or lacked a functional enteral route—introducing selection bias that could inflate the apparent benefit. The authors are appropriately cautious, framing their mortality finding as exploratory and calling for prospective, adequately controlled studies. Yet in a clinical scenario that is becoming progressively rarer as the pandemic evolves, such single-center observations may represent some of the only data we will ever gather on this particularly challenging intersection of surgery and viral infection.

Subject of Research: High-dose colchicine treatment and clinical outcomes in COVID-19 patients with surgical conditions

Article Title: High-dose colchicine and clinical outcomes in COVID-19 patients with surgical conditions: A single-center retrospective cohort study

Article References: Arabadzhieva, E., Yonkov, A., Bulanov, D., Korukov, G., Shavalov, Z., & Mitev, V. (2026). High-dose colchicine and clinical outcomes in COVID-19 patients with surgical conditions: A single-center retrospective cohort study. Pharmacia, 73, Article e212514. https://doi.org/10.3897/pharmacia.73.e212514

Image Credits: AI Generated

DOI: 10.3897/pharmacia.73.e212514

Keywords: colchicine, COVID-19, surgery, NLRP3 inflammasome, ferritin, hyperinflammation, mortality, retrospective cohort, biomarkers, perioperative outcomes, anti-inflammatory, SARS-CoV-2

The central finding is striking: the parts of the parsnip that most people throw away are precisely the parts richest in bioactive compounds. Among the edible tissues, the skin of the ‘Warrior’ cultivar recorded the highest flavonoid content, at 15.27 milligrams of catechin equivalents per 100 grams of fresh weight. Among the inedible tissues, ‘Warrior’ leaves topped the chart for phenolic content, reaching 525.17 milligrams of gallic acid equivalents per 100 grams of fresh weight. These numbers matter because phenolic compounds and flavonoids are among the most studied classes of plant secondary metabolites, valued for their capacity to neutralize reactive oxygen species and modulate inflammatory signaling pathways in human cells.

Antioxidant activity in the study was assessed using two widely accepted colorimetric assays, DPPH and ABTS, each of which measures the ability of plant extracts to scavenge synthetic free radicals in solution. The DPPH assay relies on the reduction of a stable nitrogen-centered radical, which changes color from deep purple to pale yellow as antioxidants donate electrons or hydrogen atoms. The ABTS assay works on a similar principle, generating a green-blue radical cation that is decolorized by antioxidant molecules. When the researchers ran these assays on extracts from different parsnip tissues, the results tracked closely with the distribution of phenolic compounds, reinforcing a long-standing observation in food chemistry that total phenolic content is often a reliable predictor of radical-scavenging capacity.

Cultivar differences emerged as a consistent theme throughout the data. The ‘Warrior’ cultivar generally exhibited higher total flavonoid content, higher total phenolic content, and stronger antioxidant activities than ‘Albion’ across the tissues examined. This kind of genotype-dependent variation is well documented in other vegetables; comparable studies of onions, blueberries, and aronia berries have all shown that polyphenol profiles can differ substantially between cultivars grown under identical conditions. For breeders and food scientists, the implication is that cultivar selection is not merely a matter of yield, texture, or flavor, but also a lever for enhancing the nutritional and functional value of a crop.

The anti-inflammatory experiments took the investigation a step further, moving from chemical assays into living cells. The team used RAW 264.7 macrophages, a mouse cell line that has become a standard model for studying inflammatory responses in vitro. These immune cells were stimulated with lipopolysaccharide, or LPS, a molecule derived from the outer membrane of Gram-negative bacteria that triggers a potent inflammatory response, including the production of nitric oxide and a burst of intracellular reactive oxygen species. Nitric oxide, while serving important signaling functions at low concentrations, contributes to tissue damage and inflammatory pathology when overproduced by activated macrophages, making its inhibition a key benchmark for anti-inflammatory activity.

Against this backdrop, ‘Warrior’ parsnip skin extract delivered the study’s most compelling result. The skin extract showed the strongest anti-inflammatory activity of all the tissues tested, suppressing both nitric oxide production and the generation of intracellular reactive oxygen species in the LPS-stimulated macrophages. This dual action is significant because oxidative stress and inflammation are tightly intertwined processes; reactive oxygen species can activate inflammatory signaling cascades, and inflammatory enzymes in turn generate more free radicals. Compounds that interrupt this feedback loop at both points are of particular interest to researchers exploring dietary approaches to chronic inflammatory conditions, which underlie diseases ranging from atherosclerosis to arthritis.

The concentration of bioactive compounds in outer tissues is not unique to parsnip, but the study adds a valuable quantitative dimension to a pattern seen across the plant kingdom. In apples, grapes, and onions, the peel routinely outperforms the flesh in phenolic content, a consequence of the plant’s own defensive strategy. The outer layers of a root or fruit are the first line of contact with the environment, exposed to ultraviolet radiation, pathogens, and physical damage, and plants respond by accumulating protective secondary metabolites precisely where they are needed most. Leaves, similarly, face intense oxidative pressure from photosynthesis and sunlight, which helps explain why ‘Warrior’ parsnip leaves, normally discarded as agricultural waste, turned out to be the single richest source of phenolics in the entire analysis.

That last point carries real economic and environmental weight. Parsnip is grown primarily for its taproot, and the foliage is typically left in the field or composted after harvest. If the leaves contain more than 500 milligrams of phenolic compounds per 100 grams of fresh weight, they represent a largely untapped reservoir of functional ingredients that could be recovered for use in nutraceuticals, functional foods, or natural preservatives. The same logic applies to peeling waste from food processing operations, where parsnip skins are removed on an industrial scale. Converting these by-products into value-added extracts would align with a broader movement in food science toward circular economy approaches, in which agricultural residues are reimagined as raw materials rather than refuse.

The study also situates parsnip within a growing body of literature on root vegetables as sources of health-promoting compounds. Previous work by the same research group had already characterized the physicochemical properties, organic acids, and sugar profiles of parsnip cultivars harvested in Korea, and other teams have documented the antioxidant activity of essential oils from wild parsnip subspecies. Historical texts and traditional medicine systems have long attributed therapeutic properties to Pastinaca sativa, and modern pharmacological reviews have catalogued its chemical constituents. What the new research adds is a systematic, tissue-by-tissue, cultivar-by-cultivar comparison that connects specific chemical measurements to measurable biological effects in cell-based models, bridging the gap between compositional analysis and functional validation.

For consumers, the practical takeaways are straightforward, if somewhat counterintuitive. Keeping the skin on parsnips when cooking preserves the tissue shown to have the highest flavonoid content and the strongest anti-inflammatory activity in laboratory tests, and choosing cultivars such as ‘Warrior’ may offer a modest nutritional edge over alternatives. The researchers caution, as all in vitro studies must, that cellular assays do not directly translate into clinical outcomes; compounds must survive digestion, reach target tissues, and act in the complex environment of the human body before any health benefit can be claimed. Nevertheless, the work provides a clear roadmap for future research, from identifying the individual polyphenols responsible for the observed effects to testing bioavailability and efficacy in more advanced models. In the meantime, it offers a fresh reason to reconsider one of the supermarket’s most overlooked vegetables, and a reminder that in the chemistry of plants, the parts we discard often hold the greatest treasures.

Subject of Research: Antioxidant and anti-inflammatory bioactive compound distribution in parsnip cultivars and plant parts

Article Title: Distribution of antioxidant compounds, antioxidant activities, and anti-inflammatory properties in different cultivars and plant parts of parsnip (Pastinaca sativa)

Article References: Shim, H., Jung, S. K., & Shin, Y. (2026). Distribution of antioxidant compounds, antioxidant activities, and anti-inflammatory properties in different cultivars and plant parts of parsnip (Pastinaca sativa). Food Science and Biotechnology. https://doi.org/10.1007/s10068-026-02344-0

Image Credits: AI Generated

DOI: 10.1007/s10068-026-02344-0

Keywords: parsnip, Pastinaca sativa, antioxidant, anti-inflammatory, polyphenols, flavonoids, phenolic compounds, cultivar, RAW 264.7 macrophages, nitric oxide, DPPH assay, food by-products

The research team, led by Renuka Ekka and supervised by Bharti Ahirwar, began by collecting fresh leaves from Kunkuri in the Jashpur district and having the plant formally identified by botanists at the university’s Department of Botany, where a voucher specimen was deposited for future reference. Before any biological testing could begin, the leaves underwent a full pharmacognostic workup. Thin sections of leaf and petiole were stained with safranin, mounted in glycerin and examined under the microscope, revealing a dorsiventral lamina with a single-layered upper epidermis, two to three layers of tightly packed palisade tissue and a spongy mesophyll riddled with air spaces. The petiole showed a thick collar of collenchyma, seven to nine cell layers deep, wrapped around V- or U-shaped vascular bundles sheathed in sclerenchyma, with calcium oxalate crystals scattered through the cortex.

These anatomical details matter more than they might first appear. Microscopic fingerprints, together with physicochemical parameters such as ash values, moisture content, swelling index, foaming index and extractive values, constitute the quality-control toolkit of herbal medicine. Because a plant can degrade in storage or be adulterated with inferior material, establishing a reproducible anatomical and physical profile is the first step toward turning a folk remedy into a standardized medicine. The team’s measurements of total ash, acid-insoluble ash and water-soluble ash now provide a benchmark against which future batches of kachnar leaf material can be authenticated and graded.

With the plant material authenticated, the researchers defatted the powdered leaves with petroleum ether and then ran an exhaustive ethanol extraction in a Soxhlet apparatus at 40 to 60 degrees Celsius for eight to ten hours. The dark green extract represented a yield of roughly 6.46 percent of the starting plant material. Preliminary screening confirmed the presence of alkaloids, flavonoids, saponins, tannins, proteins and carbohydrates, while glycosides and steroids were absent. Quantification proved more striking: the extract contained 446.85 milligrams of flavonoids per gram, expressed as quercetin equivalents, and 137.04 milligrams of phenolics per gram, expressed as gallic acid equivalents. Flavonoids and phenolic compounds are the chemical workhorses of plant antioxidant defense, and their abundance here hinted at potent biological activity.

Two complementary assays put that hint to the test. In the ABTS radical decolorization assay, which measures a compound’s ability to quench a stable blue-green radical cation, the extract achieved half-maximal scavenging at a concentration of 218.76 micrograms per milliliter, compared with 203.52 micrograms per milliliter for the ascorbic acid standard. The FRAP assay, which tracks the reduction of ferric iron to its ferrous form at low pH, gave a nearly identical half-maximal value of 217.59 micrograms per milliliter against 185.26 for the standard. The extract therefore fell only modestly short of pure vitamin C, a remarkable result for a crude mixture, and one that the authors attribute to the hydroxyl groups on its flavonoid payload, which donate electrons and hydrogen atoms to neutralize destructive free radicals before they can peroxidize lipids or damage DNA.

The antimicrobial results were more measured but still encouraging. Using the agar well diffusion method, the extract produced inhibition zones of 5 to 30 millimeters against Escherichia coli, and follow-up testing against Pseudomonas aeruginosa showed clear concentration-dependent activity: zones grew from 2.5 millimeters at 100 milligrams per milliliter to 8.5 millimeters at 400 milligrams per milliliter for E. coli, and from 1.0 to 5.5 millimeters for P. aeruginosa. Estimated minimum inhibitory concentrations came out at 100 milligrams per milliliter for E. coli and 50 for P. aeruginosa. The standard antibiotic tetracycline outperformed the extract, as expected, but the dose-responsive pattern supports the plant’s traditional use against infection, and the authors note that broader testing against Gram-positive organisms is needed to map the full antibacterial spectrum.

Anti-inflammatory activity was assessed with the bovine serum albumin denaturation assay, a widely used surrogate in which protection of protein structure stands in for suppression of inflammatory tissue damage. At 100 micrograms per milliliter the extract inhibited denaturation by 16.45 percent, rising to 23.28 percent at 200 and 34.21 percent at 400 micrograms per milliliter. Diclofenac sodium, the reference drug, achieved 24.6, 33.86 and 47.67 percent at the same doses. The extract trailed the drug at every concentration, yet the steep, dose-dependent curve confirmed appreciable in vitro anti-inflammatory potential, providing the experimental half of the validation the study set out to achieve.

The computational half proved even more provocative. The team docked five major kachnar flavonoids, rutin, quercetin, apigenin, kaempferol and catechin, into the catalytic pocket of cyclooxygenase-2, the enzyme whose overactivity drives prostaglandin-mediated inflammation and which diclofenac targets clinically. Every flavonoid outscored the drug. Rutin led with a binding affinity of minus 9.6 kilocalories per mole, followed by quercetin at minus 9.2, apigenin at minus 9.1 and kaempferol at minus 9.0, all well ahead of diclofenac’s minus 6.7. Rutin’s forest of hydroxyl groups forged multiple conventional hydrogen bonds with residues including Gln192, Gly354, His351, Tyr355 and Phe580, while quercetin and kaempferol anchored themselves through hydrogen bonding to Tyr130, Gly45 and Cys47 supplemented by pi-alkyl contacts with hydrophobic residues. Surface mapping of hydrogen bond donors and acceptors showed that the plant compounds complemented the binding pocket more thoroughly than diclofenac did.

Binding energy alone does not make a drug, so the researchers also ran the flavonoids through ADMET and drug-likeness prediction using SwissADME and pkCSM, screening against Lipinski’s Rule of Five. Apigenin, catechin, quercetin and kaempferol all passed, with molecular weights below 500 daltons and balanced lipophilicity between 0.53 and 3.22, and all four showed intestinal absorption above 70 percent, comparable to diclofenac. Apigenin emerged with the most favorable profile, combining moderate polarity with the highest predicted blood-brain barrier score among the flavonoids. Rutin, despite its stellar docking score, stumbled pharmacokinetically: its 610-dalton mass, high polar surface area and negative logP predicted poor absorption and negligible brain penetration, leading the authors to suggest that nano-delivery systems might rescue its bioavailability. Encouragingly, none of the compounds were predicted to inhibit the CYP3A4 or CYP2D6 metabolic enzymes, and all were flagged AMES-negative, indicating low risks of drug-drug interactions and mutagenicity.

Taken together, the study offers something rarer than another plant extract with activity in a dish: a mechanistic bridge between ethnobotanical tradition and molecular pharmacology. The same flavonoids that dominate the leaf chemistry also dominate the docking rankings, and the in vitro antioxidant, antimicrobial and anti-inflammatory results align with the computational predictions rather than sitting in isolation. The authors are careful to frame the work as a starting point rather than a finish line, calling for wider antimicrobial panels, preclinical studies and formulation development before any of these compounds reach the clinic. But the message for drug discovery is clear: when tribal healers in central India spent centuries refining their use of kachnar, they were running an experiment whose results modern science is only now learning to read, and the molecules hidden in its leaves may yet yield therapeutic leads that no laboratory would have thought to synthesize from scratch.

Subject of Research: Scientific validation of the traditional anti-inflammatory, antimicrobial and antioxidant uses of Bauhinia variegata through phytochemical analysis, in vitro assays and molecular docking

Article Title: Scientific validation of tribal medicinal claims of Bauhinia variegata (L.) through integrated In-Silico and experimental approaches

Article References: Ekka, R., & Ahirwar, B. (2026). Scientific validation of tribal medicinal claims of Bauhinia variegata (L.) through integrated In-Silico and experimental approaches. Discover Chemistry, 3(1), Article 455. https://doi.org/10.1007/s44371-026-00908-x

Image Credits: AI Generated

DOI: 10.1007/s44371-026-00908-x

Keywords: Bauhinia variegata, ethnomedicine, flavonoids, molecular docking, COX-2, ADMET, antioxidant, antimicrobial, anti-inflammatory, phytochemistry, drug discovery, tribal medicine

Wild mountain ginseng, Panax ginseng Meyer, occupies a near-mythical status across Korea, China, and Japan, where it has been harvested for centuries as a medicinal herb and health food. Its value stems from ginsenosides, a family of triterpene saponins that constitute the plant’s primary pharmacological constituents. These compounds are conventionally divided into three structural groups: the protopanaxadiol type, which includes well-studied molecules such as Rb1, Rb2, Rb3, Rd, Rg3, and Rh2; the protopanaxatriol type, encompassing Re, Rf, Rg1, Rg2, and Rh1; and the oleanolic acid type, represented by Ro and related saponins. Decades of research have attributed a remarkable spectrum of biological activities to ginsenosides, including immune enhancement, antioxidant and antibacterial effects, antidiabetic and anti-inflammatory actions, anti-aging properties, and cardioprotective and neuroprotective benefits.

The problem, of course, is supply. A wild mountain ginseng root of this age is an extraordinarily rare resource, and demand for authentic, high-quality material far exceeds what nature can provide. The research team’s strategy was to sidestep the bottleneck entirely by generating adventitious roots, roots that arise from somatic tissue rather than from seed germination, from the 150-year-old specimen, designated 150y-Mg. These cultured roots were then scaled up in 1000-liter industrial bioreactors, where they grew in Murashige and Skoog medium supplemented with 5 percent sucrose by weight and 5 milligrams per liter of indole-3-butyric acid, a synthetic auxin that promotes root growth and ginsenoside accumulation.

The central question was whether the cultured roots could genuinely be considered the same plant. To answer it, the researchers turned to SNP genotyping, a technique that reads single-nucleotide variations scattered across the genome and produces a molecular fingerprint unique to each individual. Using a panel of 192 SNP markers, they compared the original mountain ginseng with two independently analyzed adventitious root samples. The result was unambiguous: 100 percent genotype concordance across the entire panel. Of the 192 loci, 184 were homozygous, meaning both copies of the gene carried the same variant, five were heterozygous, and three produced null calls that could not be scored. Calculated across the 189 callable non-null loci, the genetic fixation rate stood at 97.4 percent, a figure that reflects the high homozygosity typical of a long-lived, likely self-purging lineage rather than any discrepancy between the parent plant and its cultured offspring.

With genetic identity confirmed, the team shifted to the metabolome, the complete inventory of small molecules that defines what a plant actually produces. Liquid chromatography coupled with mass spectrometry, or LC–MS, revealed clear chemical differences among the analyzed materials. Within the sample set examined, malonyl ginsenoside Rb2/Rb3 was detected in the original 150-year-old mountain ginseng but not in cultivated Panax ginseng, whereas ginsenosides XVII and F2 appeared in the bioreactor-grown adventitious roots but were absent from cultivated ginseng under the same analytical conditions. The authors are careful to frame these observations as comparison-specific metabolite features rather than validated authentication markers, a distinction that matters for any future attempt to certify the origin of ginseng products in the marketplace.

That caution is scientifically warranted. A single comparison between one wild specimen and one cultivated reference cannot establish whether a particular metabolite is truly characteristic of age, habitat, or lineage. Environmental conditions, developmental stage, and analytical parameters can all shift the metabolic profile of ginseng tissue. What the LC–MS data do provide is a shortlist of candidate compounds, malonyl ginsenoside Rb2/Rb3, ginsenoside XVII, and ginsenoside F2, that now deserve systematic validation across broader and independent ginseng cohorts before they could ever serve as reliable markers of wild mountain provenance.

Complementing the LC–MS work, high-performance liquid chromatography, or HPLC, quantified the ginsenoside content of the adventitious roots and revealed distinct quantitative patterns that set them apart from conventional material. The relative proportions of individual saponins matter enormously for pharmacological activity, since different ginsenosides act on different molecular targets in the human body. A culture line that skews toward particular saponin classes could, with further optimization, become a standardized source of specific bioactive molecules, something that wild-harvested roots, with their inherent variability, can never guarantee.

The biomedical potential of the bioreactor-grown roots was explored through preliminary in vitro assays. These experiments provided early evidence of two activities of considerable commercial and clinical interest: anti-inflammatory effects and the ability to stimulate the proliferation of dermal papilla cells, the specialized fibroblasts at the base of hair follicles that regulate hair growth. The dermal papilla finding in particular hints at possible applications in cosmetics and hair-loss research, an area where ginseng-derived compounds have long attracted attention. The authors emphasize, however, that these are preliminary results, and the path from a cell-culture assay to a validated therapeutic or cosmetic ingredient involves extensive further testing.

What makes this study notable is not any single result but the complete pipeline it demonstrates. A rare, irreplaceable botanical resource was captured genetically, propagated indefinitely in sterile culture, scaled to industrial volumes, verified as a true genetic match, and profiled chemically and functionally, all without the plant ever leaving the laboratory. The 1000-liter bioreactor scale is the crucial detail here: it transforms what would otherwise be a botanical curiosity into a feasible production platform. Adventitious root culture of ginseng has been explored before, but anchoring the technology to a documented 150-year-old wild genotype, with SNP-level traceability, raises the standard for authenticity in an industry plagued by adulteration and mislabeling.

The researchers are candid about the limits of the current work. The metabolite features they observed are candidates, not conclusions, and the in vitro activities require confirmation in more rigorous models. Yet the foundation they have laid, complete genetic concordance, a reproducible culture system, and a defined chemical baseline, gives the field exactly what it needs to move forward: a stable reference material against which future wild and cultivated ginseng samples can be compared. If subsequent studies validate the candidate markers across independent cohorts, the combination of SNP fingerprinting and LC–MS profiling could become a powerful authentication toolkit. And if the anti-inflammatory and dermal papilla activities hold up, the roots of a plant that took 150 years to grow in the mountains may one day be produced by the ton, its ancient chemistry preserved in stainless steel tanks rather than in vanishing forest soil.

Subject of Research: Metabolomic profiling and bioreactor production of adventitious roots from a 150-year-old wild mountain ginseng

Article Title: Metabolomic profiling and biomedical potential of adventitious roots derived from a 150-year-old mountain ginseng

Article References: Lee, H.-S., Han, J.-E., Kwon, A.-R., Son, E.-J., Park, H., Kim, M.-O., Kim, Y. J., Lee, K. Y., Yang, T.-J., Murthy, H. N., Paek, K.-Y., & Park, S.-Y. (2026). Metabolomic profiling and biomedical potential of adventitious roots derived from a 150-year-old mountain ginseng. BMC Plant Biology. https://doi.org/10.1186/s12870-026-10136-1

Image Credits: AI Generated

DOI: 10.1186/s12870-026-10136-1

Keywords: Panax ginseng, mountain ginseng, ginsenosides, adventitious roots, metabolomics, LC-MS, SNP genotyping, plant biotechnology, bioreactor, anti-inflammatory, dermal papilla cells, BMC Plant Biology

The new platform, described in the journal Materials Today Bio, is built from hyaluronic acid, a naturally occurring polysaccharide already familiar from cosmetic and biomedical applications. The key insight lies in the chemistry of crosslinking. Hyaluronic acid, with its abundant carboxyl groups, readily coordinates with multivalent cations such as calcium ions, forming a three-dimensional hydrogel network reinforced by hydrogen bonds in humid conditions. But when the gel encounters tissue fluid rich in monovalent sodium and potassium ions, ligand exchange displaces the pre-chelated calcium and the network rapidly falls apart. This dynamic, switchable coordination network gives the microneedles a rare combination of properties: enough mechanical strength to pierce the oral epithelium when dry, and near-instant disintegration once exposed to the salty microenvironment of ulcerated tissue.

The design inspiration came from nematocysts, the microscopic harpoon-like organelles that jellyfish use to discharge venom in response to osmotic pressure. To mimic this triggered-release strategy, the researchers first constructed drug-loaded nanofibers from glycyrrhizic acid, a natural saponin that self-assembles into long-range ordered structures with internal hydrophobic domains. Using a low-frequency acoustic resonance technique operating at 55 hertz, they co-assembled glycyrrhizic acid with two complementary plant-derived therapeutics: baicalein, a flavonoid that disrupts bacterial cell walls and inhibits bacterial DNA synthesis, and astaxanthin, a potent carotenoid antioxidant that scavenges reactive oxygen species and promotes tissue repair. The resulting nanofibers measured just 3 to 4 nanometers in diameter but stretched up to 5 micrometers in length, an extraordinary aspect ratio of 1250, with surface zeta potentials exceeding 40 millivolts that keep the suspensions physically stable.

Encapsulation within the nanofibers solved one of the most stubborn problems in phytochemical medicine: poor water solubility. Free baicalein and astaxanthin barely dissolve in aqueous media, but once loaded into the glycyrrhizic acid fibers their apparent solubilities rose to 775.50 and 95.16 micrograms per milliliter, corresponding to enhancements of 127.5-fold and 213.7-fold respectively. Because the nanofibers carry abundant surface carboxyl groups, they behave like anionic polymers and can themselves participate in calcium-mediated gelation, becoming woven into the hyaluronic acid matrix rather than merely suspended within it. When calcium chloride solution was added, a stable, self-healing gel formed within one minute, confirmed by scanning electron microscopy and rheological testing that revealed the characteristic thixotropic behavior of an electrostatically crosslinked network.

The finished microneedle patch, designated GA@BA&Ast MNs, was cast in polydimethylsiloxane molds using vacuum centrifugal casting. Each 10 by 10 millimeter patch carries a 15 by 15 array of needles, 600 micrometers tall with 300-micrometer bases, dimensions chosen to match the anatomy of the oral epithelium so the tips cross the stratum corneum without damaging deeper tissue. Mechanical testing showed the composite needles were 1.56 times stronger than pure hyaluronic acid microneedles, comfortably exceeding the 0.15-newton threshold required for epithelial penetration. Confocal imaging of fluorescently labeled patches confirmed uniform drug distribution throughout the tips, and in rat tissue the needles delivered their cargo to depths of at least 220 micrometers, reaching the deep epithelial layers that topical formulations cannot access.

Once inserted, the transformation was dramatic. In dissolution experiments simulating the oral environment at 37 degrees Celsius and high humidity, the needle tips vanished within 2 minutes, and quantitative analysis showed that more than 85 percent of the microneedle volume had decomposed within 20 minutes, leaving minimal remnants. Spectroscopic analysis with ATR-FTIR and X-ray photoelectron spectroscopy traced the mechanism: sodium ions from the tissue fluid infiltrate the matrix and associate with the hyaluronic acid carboxylates, initiating network rearrangement, while hyperosmotic conditions further drive hydration, swelling and diffusion. Compared with chitosan-based microneedles, the release rates of astaxanthin and baicalein were enhanced by factors of 15.49 and 596.31 respectively. Crucially, the released nanofibers were then rapidly taken up by surrounding cells: within 30 minutes, the absolute amounts of astaxanthin and baicalein absorbed by oral tissue exceeded those from chitosan microneedles by 91.71-fold and 401.47-fold.

Laboratory assays revealed how the two drugs divide the therapeutic labor. In endothelial cell models, the combined nanofibers drove a scratch-wound closure rate of 87.8 percent within 24 hours, significantly outperforming astaxanthin alone at 56.4 percent, and promoted the formation of orderly tubular networks on Matrigel, indicating robust pro-angiogenic activity. The dual-drug formulation also showed the strongest scavenging of reactive oxygen species in inflamed macrophages. On the antimicrobial front, baicalein proved to be the core active component: plate assays confirmed that the released nanofibers killed and inhibited both Escherichia coli and Staphylococcus aureus, while neither hyaluronic acid nor glycyrrhizic acid alone had significant effect. In lipopolysaccharide-stimulated macrophages, the combination produced the greatest reductions in the pro-inflammatory cytokines interleukin-6 and tumor necrosis factor-alpha among all tested groups.

The decisive test came in a rat model of oral ulceration induced by acetic acid chemical burn. Over a seven-day treatment period, ulcers treated with the full microneedle system achieved 77.3 percent wound closure, compared with just 25.5 percent natural healing in untreated animals, 34.9 percent with blank microneedles and 54.3 percent with baicalein-only patches. Macroscopically, the treated ulcers regained a healthy pink color, a sign of rapid revascularization absent in the controls. Histological examination told the same story: while untreated animals remained at the early granulation stage, the combination-treated tissue showed a smooth, continuous epithelial layer covering the wound with minimal inflammatory infiltration, hallmarks of the final maturation and remodeling phase of healing. Masson’s trichrome staining revealed uniformly organized collagen fibers resembling normal mucosa, and immunohistochemistry showed collagen deposition enhanced by 41 percent and vascular endothelial growth factor expression boosted by 47 percent relative to model controls, alongside elevated phosphorylation of PI3K and Akt, suggesting the pro-angiogenic effect runs through this well-known signaling pathway.

Safety results were equally encouraging. Major organs from treated animals showed intact architecture without inflammation, necrosis or fibrosis, the hemolysis rate stayed below the 5 percent acceptance criterion, and endothelial cell viability remained above 90 percent after exposure to patch extracts. Because the formulation relies on plant-derived compounds rather than antibiotics or corticosteroids, it sidesteps the side effects and resistance concerns associated with conventional pharmacological treatments. The researchers position the platform as a universal delivery system for hydrophobic small-molecule drugs, one whose osmolality-triggered disintegration requires no external stimulus and is tailored specifically to the wet, hyperosmotic and mechanically active environment of the mouth. If the approach translates to the clinic, the humble jellyfish sting, refined over hundreds of millions of years of evolution, may offer relief to the millions of people who suffer each year from the raw, painful lesions of oral ulcers, and potentially to patients with oral fibrosis and oral cancer as well.

Subject of Research: Osmolality-responsive dissolving microneedles for oral ulcer drug delivery

Article Title: Hyaluronic acid-based osmolality-responsive immediate-release microneedles co-loading baicalein and astaxanthin for oral ulcer therapy

Article References: Yang, J., Shi, K., Wang, J., Liu, H., Zhang, Y., Guang, X., Wang, S., Lei, W., Wang, Y., Tan, M., Ma, X., & Wu, H. (2026). Hyaluronic acid-based osmolality-responsive immediate-release microneedles co-loading baicalein and astaxanthin for oral ulcer therapy. Materials Today Bio, 41, Article 103702. https://doi.org/10.1016/j.mtbio.2026.103702

Image Credits: AI Generated

DOI: 10.1016/j.mtbio.2026.103702

Keywords: microneedles, oral ulcers, hyaluronic acid, drug delivery, baicalein, astaxanthin, glycyrrhizic acid, nanofibers, biomimetic, osmolality-responsive, wound healing, anti-inflammatory

The researchers surveyed peer-reviewed literature published through mid-2024, searching PubMed, Google Scholar, ScienceDirect and Wiley Online Library for studies combining cannabidiol with terms covering sunscreens, antioxidants, inflammation, UV radiation and skin biology. From that search, 19 studies made the final cut: four review articles, nine in vitro experiments, three animal studies, one human clinical trial and two mixed-method investigations. The authors are candid about the limits of their approach. Because this was a narrative review rather than a systematic one, they did not apply PRISMA methodology or formal risk-of-bias assessment, and they acknowledge the search may have missed relevant work, particularly non-English publications.

The most striking findings concern CBD’s antioxidant chemistry. Structurally, the molecule shares features with vitamins E and C: phenolic hydroxyl groups attached to aromatic rings that can donate hydrogen atoms to reactive oxygen species and free radicals, interrupting the chain reactions that damage lipids, proteins and DNA. CBD is also highly lipophilic, allowing it to accumulate in cell membranes and stabilize them in a manner reminiscent of vitamin E. In rat experiments, chronic UVA and UVB exposure distorted keratinocyte membrane phospholipid metabolism, and topical CBD partially reversed those changes, downregulating harmful lysophosphatidylcholines and phospholipase A2 activity while upregulating protective phosphatidylethanolamines and phosphatidylserines. In human keratinocytes stressed with hydrogen peroxide or UVB, CBD reduced malondialdehyde and 4-hydroxynonenal, two well-established markers of lipid peroxidation, and modulated proteostasis networks governing protein folding and redox balance in ways that increased cell survival.

Beyond these direct chemical effects, CBD appears to manipulate the skin’s own antioxidant machinery. The review highlights its interaction with Nrf2, a redox-sensitive transcription factor often described as the master regulator of cytoprotective gene expression. Under normal conditions Nrf2 is held inactive by its nemesis Keap1, which tags it for destruction by the proteasome. Oxidative stress disrupts this pairing, freeing Nrf2 to enter the nucleus and switch on genes encoding superoxide dismutase, glutathione peroxidase and heme oxygenase 1. Intriguingly, keratinocyte studies suggest CBD is only a weak Nrf2 activator but a strong inhibitor of BACH1, a transcriptional repressor that works alongside Nrf2 to control heme oxygenase 1. This positions CBD as an Nrf2-independent booster of HMOX1 expression, encouraging keratinocyte differentiation and cytokeratin production, processes critical to maintaining a skin barrier that resists UV-induced DNA damage.

The anti-inflammatory story runs through a different set of molecular switches. CBD appears to be a major inhibitor of NFκB signaling, the central hub of the inflammatory response. Normally locked in the cytoplasm by its inhibitor IκB, NFκB is released when pro-inflammatory signals such as tumor necrosis factor alpha trigger IκB’s degradation, allowing the transcription factor to activate genes for cytokines, chemokines and adhesion molecules. UV irradiation drives inflammation through exactly this pathway, and in three-dimensional human keratinocyte cultures CBD counteracted it, restoring IκB levels and suppressing NFκB. CBD also dampened the NLRP3 inflammasome and the pro-inflammatory protein PGAM5, while full-spectrum CBD extract showed high-affinity inhibition of NLRP3 and TGF-β1 responses. In human skin fibroblasts, CBD elevated PPARγ, a nuclear receptor that represses inflammatory pathways, and in an acne study it significantly suppressed TNF-α, IL-1β and IL-6 in human sebocytes.

The endocannabinoid system adds yet another layer. CB2 receptors, found in immune and peripheral tissues including skin, can restrain pro-inflammatory cytokine release, and CBD’s modulation of CB2, along with its desensitization of TRPV1 channels activated by oxidative stress and its activation of adenosine A2A receptors, may collectively calm overactive immune responses in UV-damaged skin. One study of patients with psoriasis, atopic dermatitis and scarring found that a CBD-enriched ointment improved disease severity, quality of life, skin hydration and elasticity with no adverse effects. The review also flags a fascinating effect on melanocytes: CBD can activate p38 and p42/44 MAPK signaling and independently upregulate MITF, tyrosinase and related proteins, enhancing melanogenesis, the production of the pigment that naturally scatters and absorbs UV radiation. This raises potential applications for hypopigmented disorders and hints at melanin-mediated photoprotection.

But here is where the enthusiasm must be tempered, and the review is refreshingly blunt about it. Spectral analyses show that CBD absorbs UV light predominantly between roughly 220 and 280 nanometers, a range overlapping UVC, which is filtered out by the atmosphere, and only minimally touching the UVB band that sunscreens must block. In one comparative study, CBD showed the strongest cytoprotection against UVA-associated injury while cannabinol performed best against UVB, but neither CBD nor its relatives demonstrated direct photoprotective absorption at the wavelengths that matter. The authors emphasize that the observed cytoprotective effects should not be interpreted as sunscreen activity. CBD’s benefits, if real, would be indirect, working beneath the filter layer to help skin cells survive whatever radiation gets through.

Safety questions also complicate the picture. Most systematic safety data come from oral CBD, where randomized trials have identified increased risks of diarrhea, somnolence, decreased appetite and abnormal liver function tests, though the hepatic and sedation signals were concentrated in high-dose childhood epilepsy studies using drugs like clobazam and valproate. CBD is metabolized by CYP450 liver enzymes and can be a potent dose-dependent inhibitor of their activity, a concern that depends heavily on how much of a topical dose actually reaches the bloodstream. Evidence on that front is mixed: in a 17-day study of 46 healthy adults, CBD was detectable in blood after repeated use of three of five commercial topical products, though concentrations were far below those from oral or inhaled use and no cognitive or physiological effects appeared. Topical tolerability data remain thin and formulation-dependent, with patch-testing studies showing selected CBD products were non-irritating and non-sensitizing in healthy adults, while a transdermal gel trial saw application-site dryness, pain and one case of irritant contact dermatitis.

There is one tantalizing human data point. A small pilot randomized trial of nanoparticle-encapsulated topical CBD, involving just 19 participants, found less erythema on treated skin after UVA irradiation, along with reductions in epidermal hyperplasia and cellular stress and aging markers. But the study measured no SPF and included no active sunscreen comparator, so it cannot speak to whether CBD would add anything to a real product. The review also raises a subtle photochemical concern: when CBD oxidizes, it can form the cannabinoid quinone HU-331, which absorbs UV near 270 and 409 nanometers and has shown topoisomerase-II inhibition and endothelial-cell apoptosis induction in non-skin experimental systems. CBD and its hydroxyquinone have also generated reactive oxygen species during mouse liver microsomal metabolism. None of this demonstrates phototoxicity in human skin, but it marks genuine toxicologic uncertainties that demand study before CBD rides around in a sun-exposed bottle.

The regulatory landscape adds a final layer of complexity. In the United States, sunscreens are regulated as over-the-counter drugs, and only zinc oxide and titanium dioxide currently meet the FDA’s Generally Recognized as Safe and Effective standard, while the 2022 Modernization of Cosmetics Regulation Act has tightened scrutiny of cosmetic ingredients, with new 2026 legislation targeting full-spectrum CBD products specifically. Any manufacturer hoping to add CBD to a sunscreen would face registration, human safety substantiation and adverse event surveillance requirements. The review’s bottom line is measured: CBD may eventually earn a role as an adjunctive, non-filter component of photoprotective skincare, but the evidence base, dominated by in vitro and rodent work with enormous variability in models and doses, is nowhere near supporting claims of sun protection. Until standardized SPF, stability, photostability and human safety testing say otherwise, your sunscreen’s active ingredients should remain the ones with proven track records.

Subject of Research: Preclinical evidence on cannabidiol's effects against ultraviolet-induced skin damage and its potential as a sunscreen additive

Article Title: Cannabidiol and ultraviolet-induced skin damage: a narrative review of preclinical evidence and translational considerations for sunscreen additive development

Article References: Papadeas, G. G., Szeto, M. D., Reed, M. J., Paul, A., Runion, T. M., Anderson, J., & Dellavalle, R. P. (2026). Cannabidiol and ultraviolet-induced skin damage: a narrative review of preclinical evidence and translational considerations for sunscreen additive development. Archives of Dermatological Research, 318(1), Article 430. https://doi.org/10.1007/s00403-026-04888-x

Image Credits: AI Generated

DOI: 10.1007/s00403-026-04888-x

Keywords: cannabidiol, CBD, sunscreen, UV radiation, photoprotection, skin cancer, antioxidant, anti-inflammatory, keratinocytes, melanocytes, Nrf2, dermatology

The study, published in Discover Chemistry, screened the Pan-African Natural Products Library, known as p-ANAPL, a curated collection of compounds derived from African medicinal plants. Rather than relying on docking scores alone, the researchers built a multi-stage pipeline that begins with ADMET filtering, which predicts how a molecule is absorbed, distributed, metabolized, excreted, and whether it poses toxicity risks. This approach acknowledges a hard truth in drug discovery: a compound that binds tightly but fails Lipinski’s Rule of Five, or blocks the hERG potassium channel critical for heart rhythm, is a dead end no matter how impressive its binding energy appears on paper.

The target protein was murine COX-2, taken from the Protein Data Bank under identifier 4PH9 at a remarkably high resolution of 1.81 angstroms. Crucially, this crystal structure contained ibuprofen bound in the active site, giving the team a known answer to validate their docking protocol. When they re-docked ibuprofen and compared the result to the original crystallographic pose, the heavy-atom root-mean-square deviation came out at just 0.85 angstroms, well below the commonly accepted 2.0 angstrom threshold. This gave the researchers confidence that their computational setup was faithfully reproducing the physics of drug binding in the COX-2 channel.

With the protocol validated, all 520 compounds in the p-ANAPL library were screened using a hierarchical approach: high-throughput virtual screening first, then standard precision docking to refine the top 33 candidates, and finally extra precision docking on the best five. Two molecules rose above the rest: 152CSB2 and Thix6g, both of which outscored ibuprofen in the extra precision ranking. The researchers emphasized that selection was not based on docking scores alone but on a combination of binding scores, interaction patterns with key residues, and ADMET acceptability, a more holistic criterion that reduces the risk of false positives.

Both lead compounds anchored themselves in the NSAID-binding channel through contacts with Arg-120 and Tyr-355, the catalytic gatekeepers that normally admit arachidonic acid. 152CSB2 formed three hydrogen bonds, including donor interactions with Arg-121 and Tyr-356 plus an acceptor bond with Met-523, along with a salt bridge to the guanidinium group of Arg-120, mirroring the classic binding mode of competitive NSAIDs. Thix6g, meanwhile, relied on two hydrogen bonds and a battery of aromatic interactions, including stacked pi-pi contacts with Tyr-356 and pi-amide contacts with Gly-527, suggesting a different but equally stabilizing strategy for occupying the pocket.

To confirm these poses were not fleeting artifacts of a static snapshot, the team ran 200-nanosecond molecular dynamics simulations using the Desmond package. The protein backbone of both complexes remained stable, with RMSD values hovering between 2.8 and 3.2 angstroms for 152CSB2 and around 3.0 to 3.2 angstroms for Thix6g. The ligand RMSD for Thix6g stayed remarkably close to its initial binding mode throughout the simulation, while 152CSB2 showed an initial adjustment period before settling into a stable configuration. Hydrophobic contacts between 152CSB2 and residues Tyr-356, Val-524, and Tyr-386 persisted for 32, 62, and 88 percent of the simulation time respectively, providing a dynamic picture of sustained binding that no single docking frame could capture.

Binding free energy calculations using the MM-GBSA method, performed on 400 equally spaced frames from the final 100 nanoseconds of trajectory, delivered the study’s most striking result. 152CSB2 posted a binding free energy of minus 32.12 kilocalories per mole, while Thix6g managed only minus 0.29 kilocalories per mole, a dramatic gulf that reflects fundamental differences in how the two molecules fit their target. The van der Waals contribution for 152CSB2 reached minus 16.97 kilocalories per mole against just minus 6.30 for Thix6g, pointing to superior steric complementarity. Thix6g was further penalized by high ligand strain energy and unfavorable desolvation costs, meaning the molecule had to contort itself into a less natural shape to squeeze into the active site.

The researchers then deployed density functional theory calculations at the B3LYP/6-311++G(d,p) level to probe the electronic personalities of the lead compounds. Both 152CSB2 and Thix6g showed lower ionization potentials than ibuprofen, meaning they donate electron density more readily, a property that could enhance their interactions with electron-poor residues in the COX-2 pocket. 152CSB2 also exhibited the smallest HOMO-LUMO gap at 0.28 atomic units, the highest softness, and the largest electrophilicity index, collectively marking it as the most electronically reactive of the three molecules. The frontier molecular orbital distribution for 152CSB2 spread across an extended aromatic system with a conjugated ethylenic bond, whereas Thix6g’s orbitals localized around oxygen-bearing phenyl groups, hinting at distinct mechanisms of electronic engagement with the protein.

Despite the promise, the authors are careful to frame these findings as computational hypotheses rather than proven drug candidates. MM-GBSA values are semi-quantitative ranking estimates, not experimentally measured affinities, and predicted ADMET profiles must be validated in the laboratory before any lead optimization can begin. The team also notes that the hierarchical HTVS-to-SP-to-XP screening workflow, though perhaps computationally unnecessary for a library of only 520 compounds, was retained as a scalable demonstration that can be applied to much larger African natural product collections in the future.

Nevertheless, the study represents a meaningful step toward harnessing Africa’s largely untapped botanical diversity for modern drug discovery. By combining rigorous structural biology, molecular dynamics, quantum chemistry, and pharmacokinetic filtering into a single pipeline, the researchers have shown that natural compounds from the continent’s medicinal plants can compete with, and in some respects outperform, blockbuster synthetic drugs like ibuprofen at the molecular level. 152CSB2, with its combination of stable binding, favorable ADMET characteristics, and distinctive electronic profile, now stands as the most compelling candidate for the in vitro and in vivo studies that will determine whether a digital lead can become a real medicine for inflammatory disease.

Subject of Research: In silico screening of the Pan-African Natural Products Library for selective COX-2 inhibitors

Article Title: In silico evaluation of p-ANAPL library against inhibiting the cognate isoform cyclooxygenase Cox-2

Article References: Gawoua Teumen, D., Amana, B. A., Eyia Andiga, L. G., Moto Ongagna, J., Amoa, P. P., Govender, K. K., & Bikele Mama, D. (2026). In silico evaluation of p-ANAPL library against inhibiting the cognate isoform cyclooxygenase Cox-2. Discover Chemistry, 3(1), Article 478. https://doi.org/10.1007/s44371-026-00924-x

Image Credits: AI Generated

DOI: 10.1007/s44371-026-00924-x

Keywords: COX-2, p-ANAPL, molecular docking, ADMET, molecular dynamics, MM-GBSA, DFT, natural products, virtual screening, anti-inflammatory, drug discovery, inflammation