In the present work, we investigated the effect of Lycium barbarum L. polysaccharides (LBPs) on L-02 cells exposed to alcohol exploring the potential molecular mechanisms. Our results suggested that LBPs significantly prevented alcohol-induced hepatotoxicity with dose-dependent effect, indicated by both cell viability and diagnostic indicators of liver damage. Moreover, alcohol induced excessive oxidative stress, as evidenced by an increase of the malondialdehyde level and reactive oxygen species production, while reducing antioxidant enzymes (T-SOD, CAT, and GPx) in liver, were inhibited by administration of LBPs. Furthermore, LBPs reversed the cell apoptosis and increased the mitochondrial membrane potential in alcohol-treated liver cell. Studies of underlying mechanisms revealed that LBPs increased expression levels of Nrf2 expression, which in turn blocked proapoptotic signaling events, restoring the balance between proapoptotic Bax and antiapoptotic Bcl-2 proteins, suppressing activities of cytochrome C (Cyto c), caspase-3, and caspase-9 in L-02 cells stimulation by ethanol. In general, the results showed that the inhibition of alcohol-caused liver damage by LBPs is due at least in part to its antioxidant and antiapoptosis activity via Nrf2 signaling pathway.
Keywords: Lycium barbarum L.; alcohol; apoptosis; oxidative damage; polysaccharide.
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