Abstract: Objective: To investigate the effect of anthocyanins from Nitraria tangutorun Bobr. fruits on nonalcoholic fatty liver injury induced by high-fat diet (HFD) in C57BL/6J mice and its underlying mechanism. Methods: Male C57BL/6J mice were randomly divided into control, model and anthocyanin treatment groups. The feeding period lasted for 14 weeks. Routine physiological parameters (body mass, abdominal fat mass, body fat index, visceral fat mass, body length and Lee’s index) were measured in each mouse. Serum samples were collected to detect the activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and the concentrations of total cholesterol (TC), total triglyceride (TG), low density lipoprotein (LDL) and high density lipoprotein (HDL). Besides, liver samples were collected to detect oxidative stress-related indicators such as malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and the expression of liver lipid metabolism-related proteins such as acetyl coenzyme A carboxylase (ACC), liver X receptor-alpha (LXR-α), fatty acid translocase (CD36) and peroxisome proliferator-activated receptor-alpha (PPAR-α). Results: Compared with the high-fat model group, the anthocyanins from N. tangutorun Bobr. significantly reduced body mass, abdominal fat mass, body fat index, visceral fat mass and Lee’s index. The levels of serum AST, ALT, TC, TG and LDL were significantly reduced and HDL level in high-fat diet-fed mice was significantly increased after administration with the anthocyanins. In addition, the anthocyanins significantly decreased MDA content and SOD activity and increased GSH-Px activity, as well as significantly downregulated the expression of ACC, LXR-α and CD36 and upregulated the expression of PPAR-α in liver tissue. Conclusion: The anthocyanins from N. tangutorun Bobr. can ameliorate HFD-induced NAFLD in mice by regulating oxidative stress and lipid metabolism in hepatocytes.

Key words: anthocyanins from Nitraria tangutorun Bobr. fruits, nonalcoholic fatty liver injury, oxidative stress, lipid metabolism