Protective effects of Lactiplantibacillus pentosus CQZC01 on alcohol-induced gastric mucosa injury in mice via an anti-oxidative mechanism

Gastric ulcer is a very common disease of the digestive system, and it is important to understand how this disease can be prevented and treated. In this study, the effects of Lactiplantibacillus pentosus CQZC01 (LP-CQZC01) on alcohol-induced gastric mucosal injury were investigated by evaluating the extent of hemorrhage and edema, as well as cell necrosis and gastric mucosal cell shedding. In addition, the levels of oxidative stress-related in-dicators, gastric mucosal defense factors, and pro-inflammatory cytokines were measured. After treatment with LP-CQZC01, the area of gastric mucosal damage was significantly reduced, and the ulcer inhibition rate and the extent of gastric mucosal damage were improved. LP-CQZC01 also significantly increased the levels of so-matostatin (SS) and prostaglandin E2 (PGE2), as well as the levels of superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GSH-Px); however, it decreased the malondialdehyde (MDA) content, thereby improving the anti-oxidant capacity. In addition, the levels of pro-inflammatory cytokines, such as interleukin (IL)-1 beta, IL-6, and tumor necrosis factor-alpha (TNF-& alpha;), were decreased, and the anti-inflammatory factor IL-10 was elevated. The results of polymerase chain reactions revealed that LP-CQZC01 activated the nuclear factor E2-related factor 2 (Nrf2) signaling pathway, thereby increasing the levels of downstream genes & gamma;-glutamyl cysteine synthetase (& gamma;-GCS), SOD, catalase (CAT), and GSH-Px. In summary, LP-CQZC01 can alleviate alcohol-induced gastric mucosal damage by increasing the levels of gastric mucosal defense factors, inhibiting oxidative stress, and suppressing inflammation. Therefore, LP-CQZC01 is a potential therapeutic agent for the prevention and treatment of alcohol-induced gastric mucosal injury.