Lactobacillus spp. reduces ethanol‑induced liver oxidative stress and inflammation in a mouse model of alcoholic steatohepatitis
- Pei-Shan Hsieh
- Ching-Wei Chen
- Yi-Wei Kuo
- Hsieh-Hsun Ho
Affiliations: Glac Biotech Co., Ltd., Tainan 74442, Taiwan, R.O.C.
- Published online on: January 7, 2021 https://doi.org/10.3892/etm.2021.9619
Copyright: © Hsieh
et al. This is an open access article distributed under the
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Alcoholic steatohepatitis (ASH) is a complex multifactorial disease that can lead to liver fibrosis and cirrhosis if not treated promptly. Alcohol‑induced oxidative stress and inflammation are the main factors that cause steatohepatitis and liver injury; however, probiotic bacteria in the gastrointestinal tract have been revealed to regulate immune responses and reduce oxidative stress, suggesting that functional probiotics could help to prevent ASH and liver injury. Despite numerous reports on the interactions between ASH and probiotics, the mechanisms underlying probiotic‑mediated liver protection remain unknown. Therefore, the aim of the present study was to screen probiotics with high antioxidant capacity and investigate the ability of different probiotic combinations to reduce alcoholic liver disease (ALD) in a mouse model. It was identified that Lactobacillus plantarum (TSP05), Lactobacillus fermentum (TSF331) and Lactobacillus reuteri (TSR332) neutralized free radicals and displayed high antioxidant activity in vitro. In addition, these three functional probiotic strains protected mice from alcohol‑induced liver injury in vivo. Mice treated with the probiotics demonstrated significantly lower alanine aminotransferase, aspartate aminotransferase and triglyceride levels, which were associated with the downregulation of the proinflammatory cytokines TNF‑α and IL‑6. Furthermore, probiotic treatment upregulated glutathione and glutathione peroxidase activity, which are bioindicators of oxidative stress in the liver. Collectively, the present results indicated that Lactobacillus strains TSP05, TSF331 and TSR332 reduced oxidative stress and inflammatory responses, thus preventing ASH development and liver injury.