Abstract
The aim of the present study was to determine whether Lactobacillus salivarius (LS) and Lactobacillus johnsonii (LJ) prevent alcoholic liver damage in HepG2 cells and rat models of acute alcohol exposure. In this study, heat-killed LS and LJ were screened from 50 Lactobacillus strains induced by 100 mM alcohol in HepG2 cells. The severity of alcoholic liver injury was determined by measuring the levels of aspartate transaminase (AST), alanine transaminase (ALT), gamma-glutamyl transferase (γ-GT), lipid peroxidation, triglyceride (TG) and total cholesterol. Our results indicated that heat-killed LS and LJ reduced AST, ALT, γ-GT and malondialdehyde (MDA) levels and outperformed other bacterial strains in cell line studies. We further evaluated these findings by administering these strains to rats. Only LS was able to reduce serum AST levels, which it did by 26.2%. In addition LS significantly inhibited serum TG levels by 39.2%. However, both strains were unable to inhibit ALT levels. In summary, we demonstrated that heat-killed LS and LJ possess hepatoprotective properties induced by alcohol both in vitro and in vivo.
Highlights
Excess alcohol intake is one of the causes of chronic liver diseases and can lead to death [1].The development of alcoholic liver disease (ALD) is complex and involves multiple steps, which include alcoholic steatosis, alcoholic hepatitis, alcoholic cirrhosis and, eventually, liver cancer [2,3].Alcohol is metabolized by alcohol dehydrogenase, and its by-products may disrupt the normal physiology of liver cells and result in injury
Lactobacillus salivarius (LS) treatment lowered the aspartate transaminase (AST) and alanine transaminase (ALT) levels by 47.5% and 55.4%, respectively (p < 0.05), whereas Lactobacillus johnsonii (LJ) treatment lowered the AST and ALT levels by 42.2% and 55.6%, respectively (p < 0.05). γ-glutamyl transferase (γ-GT), which is secreted by the liver and gallbladder, is a common biochemical marker for alcoholic liver injury, as the levels of γ-GT
We showed that heat-killed LS and LJ alleviated the elevations of ALT, AST, γ-GT, MDA and TG in rat models of acute alcohol exposure
Summary
Excess alcohol intake is one of the causes of chronic liver diseases and can lead to death [1]. Alcohol is metabolized by alcohol dehydrogenase, and its by-products may disrupt the normal physiology of liver cells and result in injury. Alcohol increases the production of oxygen reactive species and oxidative stress in the liver. Oxidative stress can cause mitochondrial damage, protein degradation and inflammation. Individuals who abuse alcohol often have ALD [6,7,8,9]. Antioxidants such as vitamin E and resveratrol have been shown, to reduce alcoholic liver damage [10,11]
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