title: Polydatin alleviates non-alcoholic fatty liver disease in rats by inhibiting             the expression of TNF-α and SREBP-1c.
abstract: 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-α (TNF-α), 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-α, and malondialdehyde and 4-hexanonenal levels were markedly suppressed by polydatin in the liver of HFD-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-α expression, lipid peroxidation level and SREBP-1c-mediated lipogenesis.
authors.affiliation: Department of Traditional Chinese Medicine, Basic Medical College, Shaanxi University of Chinese Medicine, Xianyang, Shaanxi 712046, PR China.
authors.forename: Jingming
authors.initials: J
authors.lastname: Zhang
authors.forename: Yingying
authors.initials: Y
authors.lastname: Tan
authors.forename: Fanrong
authors.initials: F
authors.lastname: Yao
authors.forename: Qi
authors.initials: Q
authors.lastname: Zhang
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002784:Cholesterol / Q000097:blood; D059305:Diet, High-Fat; D045468:Fallopia japonica / Q000737:chemistry; D064429:Fatty Acid Synthases / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005234:Fatty Liver / Q000378:metabolism / Q000473:pathology; D005960:Glucosides / Q000494:pharmacology*; D015227:Lipid Peroxidation / Q000187:drug effects; D050155:Lipogenesis / Q000235:genetics; D008099:Liver / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D065626:Non-alcoholic Fatty Liver Disease; D020011:Protective Agents / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D027343:Rhizome / Q000737:chemistry; D013230:Stearoyl-CoA Desaturase / Q000378:metabolism; D051780:Sterol Regulatory Element Binding Protein 1 / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D013267:Stilbenes / Q000494:pharmacology*; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D005230:Fatty Acids, Nonesterified; D005960:Glucosides; D020011:Protective Agents; D051780:Sterol Regulatory Element Binding Protein 1; D013267:Stilbenes; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D002784:Cholesterol; D013230:Stearoyl-CoA Desaturase; D064429:Fatty Acid Synthases; C058229:polydatin