Vitexin Attenuates Non-alcoholic Fatty Liver Disease Lipid Accumulation in High Fat-Diet Fed Mice by Activating Autophagy and Reducing Endoplasmic Reticulum Stress in Liver

Abstract

Non-alcoholic fatty liver disease (NAFLD) has become prevalent worldwide, but sufficient pharmaceutical treatments for this condition are lacking. Previous literature suggests that vitexin offers beneficial effects in the treatment of NAFLD, but the underlying mechanisms are not well understood. In this study, the in vivo effects of vitexin were investigated in high-fat-diet (HFD)-induced NAFLD mice. Liver pathology, biochemical parameters, lipid levels, hepatocyte ultrastructure, and related regulatory proteins were measured at the end of treatment. Treatment consisted of four weeks of daily administration of vitexin at a dose of 6 mg/kg of body weight. This treatment markedly improved hepatic architecture, attenuated lipid accumulation, and regulated lipid abnormalities. In addition, the treatment reduced endoplasmic reticulum (ER) stress, restored mitochondrial biological proteins, and increased autophagy. Furthermore, the treatment increased peroxisome proliferator-activated receptor-γ (PPAR-γ) protein, which was inhibited by HFD. Thus, it was speculated that vitexin degraded lipids in HFD-induced NAFLD mice liver by inducing autophagy and restoring both ER and mitochondrial biological proteins.