Lactobacillus plantarum LC27 and Bifidobacterium longum LC67 simultaneously alleviate ethanol-induced gastritis and hepatic injury in mice

- B. longum LC67 and L. plantarum LC27 inhibited ethanol-induced NF-κB activation in KATO III cells.
- LC27 and LC67 suppressed ethanol-induced gastritis in mice.
- LC27 and LC67 reduced ethanol-induced blood ALT, AST, and TNF levels in mice.
- LC27 and LC67 increased ethanol-suppressed liver ADH and ALDH activities.
- The combination of LC27 and LC67 additively or synergistically attenuated ethanol-induced gastritis and liver injury markers.

Some probiotics attenuate ethanol-induced gastritis or liver injury. However, it is not clear whether probiotics could simultaneously alleviate ethanol-induced gastritis and liver injury. Therefore, we isolated anti-inflammatory probiotics Bifidobacterium longum LC67 and Lactobacillus plantarum LC27 in vitro and investigated their inhibitory effects against ethanol-induced gastritis and liver injury in mice. Oral administration of LC27 or LC67 suppressed ethanol-induced hemorrhagic ulcerative lesions area, myeloperoxidase activity, tumor necrosis factor (TNF) expression, CXCL4, and NF-κB activation in the stomach as well as alanine aminotransferase, aspartate transaminase, and TNF levels in the blood. Treatment with LC27 or LC67 increased ethanol-suppressed alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH) activities in the liver. The mixture of LC27 and LC67 additively attenuated ethanol-induced gastritis and liver injury in mice. These findings suggest that LC27 and LC67 can simultaneously attenuate ethanol-induced gastritis and liver injury by inhibiting inflammatory responses and increasing ADH and ALDH activities.