title: Tea polyphenols inhibit expressions of iNOS and TNF-alpha and prevent lipopolysaccharide-induced liver injury in rats.
abstract: BACKGROUND
  Tea polyphenols have been shown to protect against carbon tetrachloride (CCl4)-induced liver injury, liver fibrosis, hepatic ischemia-reperfusion injury. In this study, we examined the effect of tea polyphenols on lipopolysaccharide (LPS)-induced liver injury, and explored its mechanisms.
  
  
  METHODS
  Sprague-Dawley rats received tea polyphenols (100 mg.kg-1.d-1) or vehicle (water) intragastrically by gavage for 14 days, followed by LPS (5 mg/kg) or saline injection intraperitoneally. Liver injury was assessed by biochemical assay and pathological analysis. Serum tumor necrosis factor-alpha (TNF-alpha) levels and liver malondialdehyde (MDA) contents were determined. Inducible nitric oxide synthase (iNOS) protein and TNF-alpha, iNOS and endothelial nitric oxide synthase (eNOS) mRNA expressions in the liver were detected by immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR), respectively.
  
  
  RESULTS
  Administration of LPS resulted in liver injury in rats, evidenced by elevated activities of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST), hepatocellular necrosis, and neutrophil infiltration in the liver. These responses were associated with increased serum TNF-alpha levels, induced iNOS protein, expressions of TNF-alpha, iNOS mRNA in the liver and elevated lipid peroxidation at 90 minutes or 6 hours after LPS injection. Pretreatment with tea polyphenols attenuated LPS-induced liver injury, and blunted the rises of serum TNF-alpha levels and lipid peroxidation and the induction of expressions of TNF-alpha, iNOS in the liver.
  
  
  CONCLUSIONS
  Tea polyphenols prevent LPS-induced liver injury, and the mechanisms may involve the reduction of serum TNF-alpha levels and lipid peroxidation and the suppression of TNF-alpha, iNOS expressions in the liver.
authors.affiliation: Department of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan 430060, China.
authors.forename: Guang-Jin
authors.initials: GJ
authors.lastname: Yuan
authors.forename: Zuo-Jiong
authors.initials: ZJ
authors.lastname: Gong
authors.forename: Xiao-Mei
authors.initials: XM
authors.lastname: Sun
authors.forename: Shi-Hua
authors.initials: SH
authors.lastname: Zheng
authors.forename: Xi
authors.initials: X
authors.lastname: Li
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001483:Base Sequence; D001707:Biopsy, Needle; D056486:Chemical and Drug Induced Liver Injury; D004195:Disease Models, Animal; D005419:Flavonoids / Q000494:pharmacology*; D007150:Immunohistochemistry; D008070:Lipopolysaccharides; D008099:Liver / Q000187:drug effects* / Q000378:metabolism*; D008107:Liver Diseases / Q000473:pathology*; D008111:Liver Function Tests; D008297:Male; D008969:Molecular Sequence Data; D052247:Nitric Oxide Synthase Type II / Q000187:drug effects / Q000378:metabolism*; D010636:Phenols / Q000494:pharmacology*; D059808:Polyphenols; D011336:Probability; D012333:RNA, Messenger / Q000032:analysis; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012680:Sensitivity and Specificity; D046509:Tissue Culture Techniques; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects / Q000378:metabolism*
chemical_list: D005419:Flavonoids; D008070:Lipopolysaccharides; D010636:Phenols; D059808:Polyphenols; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D052247:Nitric Oxide Synthase Type II