Lactic acid bacteria isolated from kimchi, the staple Korean fermented vegetable dish, may offer a powerful and strain-specific shield against acute gastric injury, according to a new study published in Food Science of Animal Resources. Researchers in South Korea systematically compared three bacterial strains and found that each one substantially reduced stomach damage in rats exposed to a harsh cocktail of ethanol and hydrochloric acid, the standard laboratory mimic of alcohol- and acid-driven ulceration. In one case, the bacterial pretreatment outperformed omeprazole, the proton pump inhibitor that is one of the most widely prescribed gastric medications in the world. The findings arrive at a moment when clinicians are increasingly wary of the long-term risks of acid-suppressing drugs, including associations with kidney disease, and are searching for food-derived alternatives that can shore up the stomach’s own defenses rather than simply switching off acid production.
The research team, led by investigators at Chonnam National University in collaboration with Nong Shim Co. Ltd. and Dongshin University, began with a large-scale screening effort. Thirty-seven lactic acid bacteria strains maintained in their laboratory were tested for the two traits that any probiotic hoping to survive the journey to the stomach must possess: tolerance to strongly acidic conditions and resistance to bile. The bacteria were incubated in buffers adjusted to pH 2.0, 2.5, and 3.0, and separately in growth medium containing 0.5 percent Oxgall, a purified bovine bile preparation. Viable cell counts, expressed as log colony-forming units per milliliter, revealed dramatic differences. At pH 2.0, one strain retained nearly 4.89 log CFU/mL while two common dairy strains, Lacticaseibacillus casei and Limosilactobacillus reuteri, were wiped out entirely. From this gauntlet, seven strains emerged, and three were advanced for full evaluation: Lacticaseibacillus rhamnosus NS2301G1, Limosilactobacillus fermentum NS2301G2, and Levilactobacillus brevis NS2301G3, all originally isolated from kimchi.
Safety testing preceded any therapeutic claims. The three strains were profiled for antibiotic susceptibility using Etest strips against nine clinically relevant antibiotics, including ampicillin, vancomycin, gentamicin, erythromycin, and tetracycline, with minimum inhibitory concentrations interpreted against the microbiological cut-off values published in current European Food Safety Authority guidance. All measured values fell at or below the applicable thresholds. Hemolytic activity, a key virulence concern for any bacterium proposed for consumption, was assessed on blood agar plates, and all three strains displayed gamma-hemolysis, meaning no red blood cell destruction whatsoever. These results position the strains as credible candidates for incorporation into functional foods rather than merely as laboratory curiosities.
Before moving into animals, the team tested the bacteria against human gastric epithelial cells. NCI-N87 cells, a widely used human stomach cancer-derived epithelial line, were pretreated for six hours with each live bacterial suspension at one million colony-forming units per milliliter and then assaulted with a solution of 5 percent ethanol in 10 millimolar hydrochloric acid. The corrosive treatment alone drove cell viability down to roughly 60 percent of untreated controls. Pretreatment with the bacteria pulled viability back to between 89 and 102 percent, with NS2301G2 and NS2301G3 effectively restoring survival to control levels and exceeding the protection offered by omeprazole, which reached 88 percent. The protection was accompanied by molecular changes: the chemical assault slashed expression of MUC5AC, the gene encoding the gel-forming mucin that forms the stomach’s viscoelastic protective lining, by nearly 70 percent, along with DEFB4B, an inducible beta-defensin involved in antimicrobial defense, and PTGER3, a prostaglandin receptor gene tied to mucosal protection. Bacterial pretreatment significantly blunted or reversed all three losses.
The decisive experiment took place in living animals. Thirty male Sprague-Dawley rats were divided into six groups and received daily oral doses for fourteen days: phosphate-buffered saline for the control and injury groups, omeprazole at 20 milligrams per kilogram, or one of the three bacterial strains at one billion colony-forming units per animal per day. On the final day, after a 24-hour fast, all animals except the controls received two milliliters of 60 percent ethanol containing 150 millimolar hydrochloric acid by oral gavage. One hour later, the stomachs were harvested and the hemorrhagic lesion area quantified using image analysis software. The untreated injury group developed lesions covering 24.2 square millimeters, or about 21.4 percent of the total gastric surface. Pretreatment shrank that damage dramatically: omeprazole reduced lesions to 7.8 square millimeters, NS2301G1 to 10.5, NS2301G2 to 13.1, and NS2301G3 to just 6.2 square millimeters, meaning the L. brevis strain protected the stomach better than the blockbuster acid-suppressing drug itself.
Histological examination under the microscope confirmed what the naked eye suggested. Stomach sections from the injury group showed devastated glandular architecture, epithelial cell necrosis, mucosal erosion, focal hemorrhage, and dense inflammatory infiltration. In contrast, tissues from bacteria-treated rats retained comparatively preserved glandular structures with far less necrosis and bleeding, findings evaluated by a pathologist blinded to group allocation. Western blot analysis of the tissue proteins added a mechanistic layer: the injury group showed markedly elevated interleukin-6, a pro-inflammatory cytokine, alongside sharply depressed MUC5AC protein, the workhorse mucin of the gastric mucus barrier. Bacterial pretreatment suppressed IL-6 and preserved MUC5AC, indicating that the bacteria were not merely diluting the insult but actively reprogramming the stomach’s inflammatory and barrier-maintenance machinery.
Quantitative PCR on gastric tissue deepened the molecular picture. Ethanol and hydrochloric acid exposure cut Muc5ac messenger RNA nearly in half and reduced the anti-inflammatory cytokine gene Il10 by about 54 percent, while driving pro-inflammatory mediators into overdrive: Ptgs2, the gene encoding cyclooxygenase-2, rose almost 89 percent, Il6 surged nearly fivefold, and Tnf nearly doubled. The bacterial treatments partially reversed every one of these shifts. NS2301G1 proved the strongest all-around performer, restoring Muc5ac to 0.82 normalized units and pushing Il10 to 1.38 while suppressing Il6 more effectively than its counterparts. Serum cytokine measurements told a parallel story of systemic protection: injury rats showed TNF-alpha climbing from about 16 to 118 picograms per milliliter, yet NS2301G1-treated animals capped the surge at roughly 41 picograms per milliliter, with IL-6 showing a similar attenuation across all three bacterial groups.
Why did closely related bacteria perform so differently? The authors turned to previously published genome sequences of the three strains for clues. All three share a core toolkit of glutathione- and thioredoxin-associated redox defense genes, including gshAB, trxA, trxB, and tpx, suggesting a common capacity to withstand oxidative stress, a central driver of ethanol-induced mucosal damage. But the strain-specific extras are telling. NS2301G1 uniquely carries bsaA, encoding glutathione peroxidase, and npr, encoding NADH peroxidase, an apparent added capacity for peroxide detoxification that may underpin its strong anti-inflammatory performance. NS2301G3 stands apart with katA, a catalase gene, and a complete glutamate decarboxylase system, gadB and gadC, which consumes intracellular protons to convert glutamate into gamma-aminobutyric acid, conferring exceptional acid resistance, a plausible explanation for its unmatched reduction of macroscopic lesions under the brutal acid challenge. The researchers are careful to note that genomic annotation alone does not prove expression or causation, and they frame these candidates as hypotheses demanding transcriptomic and metabolomic follow-up.
The broader implications reach from the clinic to the dairy aisle. Proton pump inhibitors, while effective, have drawn mounting scrutiny over associations with acute and chronic kidney disease and concerns about long-term use, and resistance complicating Helicobacter pylori eradication continues to erode conventional options. Lactic acid bacteria offer an appealing alternative strategy: rather than suppressing acid, they reinforce the mucosal mucus barrier, temper inflammatory signaling, and bolster antioxidant defenses, all through organisms with an established safety record in fermented foods. Because these particular strains are acid- and bile-tolerant kimchi isolates, they are natural candidates for fermented dairy products and other animal-derived food matrices, where they could deliver gastroprotective benefits alongside nutrition. The study’s authors emphasize that their findings, while striking, come from an acute animal model, and that human trials, technological characterization as starter cultures, and identification of the precise bacterial components responsible remain the essential next steps before a kimchi-derived probiotic could become a mainstream prescription for stomach health.
Subject of Research: Comparative gastroprotective effects of lactic acid bacteria strains against ethanol/HCl-induced gastric injury
Article Title: Comparative evaluation of the gastroprotective effects of lactic acid bacteria strains against ethanol/HCl-induced gastric injury
Article References: Kim, K., Pyeon, M., Shin, S., Lee, J., Jeon, S., Son, B., Kim, J. H., Lee, G., Lee, J. H., & Oh, S. (2026). Comparative evaluation of the gastroprotective effects of lactic acid bacteria strains against ethanol/HCl-induced gastric injury. Food Science of Animal Resources, 46(1), Article 103. https://doi.org/10.1007/s44463-026-00109-1
Image Credits: AI Generated
DOI: 10.1007/s44463-026-00109-1
Keywords: lactic acid bacteria, probiotics, gastric injury, kimchi, gastric mucosa, ethanol-induced ulcer, omeprazole, MUC5AC, inflammation, Lactobacillus, functional foods, gastroprotection
Cite Scienmag News
Alan Morgan. (September 20, 2026). Kimchi Probiotics Shield the Stomach From Alcohol Damage in Rat Study. Scienmag. https://scienmag.com/kimchi-probiotics-shield-the-stomach-from-alcohol-damage-in-rat-study/
Alan Morgan. "Kimchi Probiotics Shield the Stomach From Alcohol Damage in Rat Study." Scienmag, 20 September 2026, https://scienmag.com/kimchi-probiotics-shield-the-stomach-from-alcohol-damage-in-rat-study/. Accessed 20 September 2026.
Alan Morgan. "Kimchi Probiotics Shield the Stomach From Alcohol Damage in Rat Study." Scienmag. September 20, 2026. https://scienmag.com/kimchi-probiotics-shield-the-stomach-from-alcohol-damage-in-rat-study/

