title: [Effects of polydatin on ALT, AST, TNF-alpha, and COX-2 in sepsis model mice].
abstract: OBJECTIVE
  To investigate the protective effects of polydatin on sepsis-induced acute liver injury (ALI) in mice, and to preliminarily study its mechanisms.
  
  
  METHODS
  The sepsis model was established using cecal ligation and puncture (CLP).A sham-operation control group was also set up. Polydatin (50, 100, and 300 mg/kg, respectively) was administrated to mice 1 h before CLP. The survival and liver injury were evaluated subsequently per 6 h after CLP. The survived mice were scarified 24 h later. The serum and the liver tissue sample were collected. The serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were detected by colorimetric method. The content of tumor necrosis factor-alpha (TNF-alpha) was assayed by ELISA. The cyclooxygenase-2 (COX-2) expression in the liver tissue was detected by Western blot. The pathological changes of the hepatic tissue were analyzed by hematoxylin and eosin stain.
  
  
  RESULTS
  The mortality of mice reached as high as 50% at 24 h after CLP. The biochemical indices and the pathological changes of the liver tissue showed obvious lesion. The success rate of modeling was 90%. Compared with the sham-operation control group, the serum ALT,AST activity, the TNF-alpha content, and the hepatic COX-2 protein expression markedly increased in the CLP group (P < 0.01). Polydatin improved the sepsis-induced mortality dose-dependently, inhibited increased ALT, AST activity and TNF-alpha, decreased the hepatic COX-2 protein expression, and attenuated the pathological injury of the liver (P < 0.05).
  
  
  CONCLUSIONS
  Polydatin could effectively protect sepsis-induced ALI, which might be achieved possibly through inhibiting serum TNF-alpha production and hepatic COX-2 expression.
authors: Chongqing Key Lab of Biochemistry and Molecular Pharmacology, Chongqing Medical University, Chongqing (400016), China.
authors: Xiao-Hui
authors: XH
authors: Li
authors: Meng-Jiao
authors: MJ
authors: Wu
authors: Li-Na
authors: LN
authors: Zhang
authors: Jia-Jia
authors: JJ
authors: Zheng
authors: Li
authors: L
authors: Zhang
authors: Jing-Yuan
authors: JY
authors: Wan
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D051546:Cyclooxygenase 2 / Q000378:metabolism; D004195:Disease Models, Animal; D005960:Glucosides / Q000494:pharmacology*; D008099:Liver / Q000201:enzymology; D051379:Mice; D008815:Mice, Inbred Strains; D018805:Sepsis / Q000378:metabolism* / Q000473:pathology; D013267:Stilbenes / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D005960:Glucosides; D013267:Stilbenes; D014409:Tumor Necrosis Factor-alpha; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; C058229:polydatin