Lactobacillus plantarum HFY09 alleviates alcohol-induced gastric ulcers in mice via an anti-oxidative mechanism.
Ya WuHong ChenYujie ZouRuokun YiJianfei MuHuayi SuoPublished in: Journal of food biochemistry (2021)
The protective effect of Lactobacillus plantarum HFY09 (LP-HFY09) on alcohol-induced gastric ulcers was investigated. Gastric morphology observation and pathological tissue sections showed that LP-HFY09 effectively relieved gastric tissue injury. The biochemical indicator detection showed that LP-HFY09 increased superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione (GSH), prostaglandin E2 (PGE2), and somatostatin (SS) levels, and decreased malondialdehyde (MDA) levels. Moreover, LP-HFY09 inhibited the levels of inflammatory cytokines interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α), and elevated the level of anti-inflammatory cytokine IL-10. The quantitative polymerase chain reaction (q-PCR) examination revealed that LP-HFY09 enhanced the mRNA expression of nuclear factor E2-related factor 2 (Nrf2) and downstream genes, including copper/zinc superoxide dismutase (SOD1), heme oxygenase-1 (HO-1), gamma-glutamylcysteine synthetase (GSH1), manganese superoxide dismutase (SOD2), catalase (CAT), and GSH-Px. This study indicated that LP-HFY09 alleviated alcohol-induced gastric ulcers by increasing gastric mucosa defense factor, and inhibiting oxidative stress and the inflammatory response. PRACTICAL APPLICATIONS: LP-HFY09 has the potential to be investigated as a treatment for gastric injury induced by alcohol.
Keyphrases
- oxidative stress
- diabetic rats
- nuclear factor
- inflammatory response
- high glucose
- hydrogen peroxide
- anti inflammatory
- fluorescent probe
- alcohol consumption
- toll like receptor
- drug induced
- type diabetes
- signaling pathway
- high resolution
- genome wide
- dna methylation
- metabolic syndrome
- climate change
- dna damage
- skeletal muscle
- nitric oxide
- quantum dots
- ischemia reperfusion injury
- genome wide analysis
- loop mediated isothermal amplification
- cell cycle arrest