Attenuation of chronic‐binge alcohol‐induced liver injury by Lactobacillus rhamnosus GG culture supernatant via inhibition of intestinal barrier dysfunction (653.12)

Abstract

Binge drinking after chronic alcohol consumption is one of the important factors contributing to the progression of hepatic steatosis to steatohepatitis. Our previous study showed that Lactobacillus rhamnosus GG (LGG) culture supernatant (LGGs) ameliorated acute alcohol‐induced liver injury. The present study investigated the effects and potential mechanisms of LGGs on chronic‐binge alcohol‐induced liver injury. Mice were fed Lieber DeCarli diet containing 5% alcohol for 4 weeks, then gavaged single dose of alcohol at 5 g/kg and lasted for 6 hours. Chronic‐binge alcohol exposure induced marked increase in hepatic steatosis and injury, which were attenuated by LGGs supplementation. LGGs application prevented chronic‐binge alcohol‐elevated intestinal permeability and circulating endotoxin level, indicating a beneficial effect of LGGs on intestinal barrier integrity. Further studies demonstrated that the effect of LGGs is through increasing intestinal tight junction proteins and proteins involved in the barrier homeostasis, such as ZO‐1, occludin, p‐glycoprotein, HIF‐2a and intestinal trefoil factor. LGGs also inhibited intestinal microRNA 122a expression, which has been shown to decrease occludin protein translation. In summary, LGGs is effective in preventing chronic‐binge alcohol‐induced liver injury by improving intestinal barrier function.Grant Funding Source: Supported by NIH, DOD and Veterans Administration