[Protective effects of polysaccharides on alcohol-induced injury of HepG2 cells and its mechanisms].

To investigate the protective effects of polysaccharides (POP) on alcohol-induced injury of HepG2 cells and its potential molecular mechanisms. After screening the appropriate concentration of alcohol-treated HepG2 cells and the intervention concentration of POP by MTT method, HepG2 cells were divided into three groups according to different intervention concentrations (200 μg/L, 400 μg/L and 600 μg/L) of POP, and the blank group without POP. After pretreated for 1 h, HepG2 cells were treated with 4% alcohol for 24 h. The activities of intracellular alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured, and the levels of intracellular reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), interleukin-1β (IL-1β) and tumor necrosis factor α (TNF- α) were measured. The protein expressions of Kelch-like epichlorohydrin-associated protein-1 (Keap1), phosphorylated nuclear factor E2-related factor 2 (p-Nrf2), phosphoamide adenine dinucleotide quinone oxidoreductase -1 (NQO1), B lymphocyte tumor-2 (Bcl-2), Bcl-2-associated X protein (Bax) and caspase 3 were detected. Compared with the HepG2 cells treated with 4% alcohol, POP at the various concentrations could effectively down-regulate the activities of ALT and AST in HepG2 cells induced by alcohol (＜0.05). The levels of IL-1β and TNF-α in the 200 μg/L POP treated group were decreased significantly (＜0.05), while the level of GSH was increased significantly (＜0.01). The levels of ROS, MDA, IL-1β and TNF-α in the 400 μg/L and 600 μg/L POP treated groups were decreased significantly (＜0.05 or ＜0.01), while the GSH level was increased significantly (＜0.01). POP effectively up-regulated the expressions of p-Nrf2 and NQO1 protein in HepG2 cells induced by alcohol, and also down-regulated the Bax/Bcl-2 index (＜0.05), and inhibited the protein expressions of Keap1 and cleaved-caspase-3 (＜0.05). POP can improve alcohol-induced oxidative stress injury in HepG2 cells by regulating the Nrf2/Keap1 pathway, thereby reducing the inflammatory index and apoptosis level of HepG2 cells. Among them, 400 μg/L and 600 μg/L POP have better intervention effects.