Levilactobacillus brevis MG5311 Alleviates Ethanol-Induced Liver Injury by Suppressing Hepatic Oxidative Stress in C57BL/6 Mice.
Hyunna JungSohyeon YouSoo-Im ChoiChang Ho KangHwan Hee LeePublished in: Microorganisms (2022)
Alcoholic liver disease (ALD), caused by excessive alcohol consumption, leads to high mortality. We investigated the hepatoprotective effect of Levilactobacillus brevis MG5311 in C57BL/6 mice with liver injuries induced by chronic ethanol plus binge feeding. L. brevis MG5311 was administered orally at a dose of 1 × 10 9 CFU/mouse once daily for 32 days. L. brevis MG5311 administration significantly reduced serum ALT, AST, and triglyceride (TG) levels in ethanol-fed mice. L. brevis MG5311 also decreased malondialdehyde levels and increased glutathione peroxidase (GPx) activity in liver tissues. In addition, hepatic TG content and histopathological scores were significantly reduced. L. brevis MG5311 increased the protein expression of SIRT1, PPARα, SOD1, CAT, and GPx 1/2 in liver tissue, while inhibiting CYP2E1 and SREBP-1c. These results indicated that L. brevis MG5311 alleviated ethanol-induced liver injury by inhibiting hepatic oxidative stress and promoting lipid metabolism. Therefore, L. brevis MG5311 may be a useful probiotic candidate for ameliorating or preventing ALD.
Keyphrases
- oxidative stress
- alcohol consumption
- diabetic rats
- type diabetes
- signaling pathway
- high fat diet induced
- dna damage
- ischemia reperfusion injury
- gene expression
- risk factors
- cardiovascular events
- cardiovascular disease
- drug induced
- coronary artery disease
- endothelial cells
- high glucose
- mass spectrometry
- induced apoptosis
- hydrogen peroxide
- body mass index
- heat shock protein
- amyotrophic lateral sclerosis