title: Hepatoprotective effects of geniposide in a rat model of nonalcoholic steatohepatitis.
abstract: OBJECTIVE
  Nonalcoholic steatohepatitis (NASH), a metabolic disorder of the liver, may gradually evolve into fibrosis or cirrhosis. Recent studies have suggested that geniposide can effectively inhibit experimental liver fibrosis. Therefore, the aim of this study was to determine whether geniposide can influence the early phase of fibrogenesis in an animal model of NASH.
  
  
  METHODS
  Male Sprague-Dawley rats were given a high fat diet alone or the same diet combined with geniposide at doses of 25, 50 or 100 mg/kg for six weeks. Ten rats received corresponding solvent as a normal control.
  
  
  RESULTS
  Treatment with geniposide could improve liver histology through reducing the elevated liver index (liver weight/body weight), serum alanine aminotransferase and aspartate aminotransferase. Total cholesterol, triglycerides and free fatty acids in serum and liver decreased in geniposide-treated rats. Furthermore, geniposide increased serum insulin levels but reduced serum tumour necrosis factor-α level in high-fat diet rats. In addition, geniposide suppressed expression of CYP2E1 and increased peroxisome proliferator-activated receptor-α (PPARα) expression. These benefits may be associated with increased superoxide dismutase and decreased malondialdehyde in liver.
  
  
  CONCLUSIONS
  Geniposide exerts protective effects against hepatic steatosis in rats fed with a high fat diet; the underlying mechanism may be associated with its antioxidant actions or regulation of adipocytokine release and expression of PPARα.
authors.affiliation: Department of Pharmacy, Anhui Medical University, Hefei bHefei XinFeng Co. Ltd, Hefei, Anhui 230032, China.
authors.forename: Taotao
authors.initials: T
authors.lastname: Ma
authors.forename: Cheng
authors.initials: C
authors.lastname: Huang
authors.forename: Guojun
authors.initials: G
authors.lastname: Zong
authors.forename: Dajun
authors.initials: D
authors.lastname: Zha
authors.forename: Xiaoming
authors.initials: X
authors.lastname: Meng
authors.forename: Jun
authors.initials: J
authors.lastname: Li
authors.forename: Wenjian
authors.initials: W
authors.lastname: Tang
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D001219:Aspartate Aminotransferases / Q000097:blood; D019392:Cytochrome P-450 CYP2E1 / Q000096:biosynthesis; D004041:Dietary Fats / Q000009:adverse effects; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004353:Drug Evaluation, Preclinical; D005234:Fatty Liver / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control; D007328:Insulin / Q000097:blood; D039823:Iridoids / Q000494:pharmacology* / Q000627:therapeutic use*; D050356:Lipid Metabolism / Q000187:drug effects; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D065626:Non-alcoholic Fatty Liver Disease; D047493:PPAR alpha / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D000893:Anti-Inflammatory Agents; D004041:Dietary Fats; D007328:Insulin; D039823:Iridoids; D047493:PPAR alpha; D014409:Tumor Necrosis Factor-alpha; C007835:geniposide; D008315:Malondialdehyde; D019392:Cytochrome P-450 CYP2E1; D013482:Superoxide Dismutase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase