Polydatin alleviates non-alcoholic fatty liver disease in rats by inhibiting the expression of TNF-α and SREBP-1c

The pathophysiology of non-alcoholic fatty liver disease remains incompletely elucidated, and available treatments are not entirely satisfactory. Polydatin, a stilbenoid compound derived from the rhizome of Polygonum cuspidatum, has been recognised to possess hepatoprotective and anti-inflammatory activities. The purpose of the present study was to determine whether polydatin has a protective effect against hepatic steatosis induced by a high-fat diet (HFD) and to elucidate its underlying molecular mechanisms in rats. Male Sprague-Dawley rats were randomly divided into four groups, including normal control, HFD model and polydatin-treated groups with polydatin levels of 30 and 90 mg/kg. Following the experimental period, plasma total cholesterol (TC), triglyceride (TG) and hepatic lipid concentrations were determined. To identify a possible mechanism, we examined the changes in liver tumor necrosis factor-alpha (TNF-alpha), lipid peroxidation levels and sterol-regulatory element binding protein (SREBP-1c) mRNA and its target genes. Both 30 and 90 mg/kg polydatin treatment alleviated hepatic steatosis and reduced plasma and liver TG. TC and free fatty acid (FFA) concentration significantly in HFD rats. In addition, TNF-alpha, and malondialdehyde and 4-hexanonenal levels were markedly suppressed by polydatin in the liver of HE'D-fed rats. Polydatin also decreased the gene expression of SREBP-1c and its target genes involved in lipogenesis, including fatty acid synthase (FAS) and stearoly-CoA desaturase 1 (SCD1) in HFD-fed rats. These results suggest that the protective effects of polydatin against HFD-induced hepatic steatosis may be partly associated with reduced liver TNF-alpha expression, lipid peroxidation level and SREBP-1c-mediated lipogenesis.