title: Protective effects of taurine against endotoxin-induced acute liver injury after hepatic ischemia reperfusion.
abstract: Hepatic ischemia reperfusion (HIR) not only results in liver injury, but also leads to endotoxemia, which aggravates HIR-induced liver injury and dysfunction, or even causes liver failure. Taurine has been shown to protect organs from ischemia reperfusion or endotoxin by its anti-oxidant and anti-inflammatory activities. The aim of this study was to investigate whether taurine could attenuate endotoxin-induced acute liver injury after HIR. Wistar rats subjected to 30 min of hepatic ischemia followed by reperfusion and lipopolysaccharide (LPS) (0.5 mg/kg) administration, exhibited liver dysfunction (elevated serum levels of ALT, AST and LDH) and hepatic histopathological alteration. The serum levels of TNF-alpha and production of myeloperoxidase (MPO) and malondialdehyde (MDA) in liver tissues and apoptosis of hepatocytes were also increased after the combination of HIR and LPS. However, pre-administration of taurine protected livers from injury induced by the combination of HIR + LPS as the histological score, apoptotic index, MPO activity and production of MDA in liver tissues, and serum levels of AST, ALT, LDH and TNF-alpha, were significantly reduced. The expression of caspase-3, Fas and Fas ligand was upregulated in homogenates of livers from rats subjected to HIR and LPS, and this elevated expression could be inhibited by taurine. In summary, the results further emphasize the potential utilization of taurine in protecting livers against endotoxin-induced injury especially after HIR, by its anti-inflammatory, anti-oxidative and anti-apoptotic activities.
authors.affiliation: Department of General Surgery, The Fifth Affiliated Hospital of Harbin Medical University, Daqing, Heilongjiang Province, China.
authors.forename: Feng
authors.initials: F
authors.lastname: Zhang
authors.forename: Yahong
authors.initials: Y
authors.lastname: Mao
authors.forename: Haiquan
authors.initials: H
authors.lastname: Qiao
authors.forename: Hongchi
authors.initials: H
authors.lastname: Jiang
authors.forename: Haifeng
authors.initials: H
authors.lastname: Zhao
authors.forename: Xiaoning
authors.initials: X
authors.lastname: Chen
authors.forename: Liquan
authors.initials: L
authors.lastname: Tong
authors.forename: Xueying
authors.initials: X
authors.lastname: Sun
mesh_terms: D000818:Animals; D053148:Caspase 3 / Q000378:metabolism; D004731:Endotoxins / Q000633:toxicity*; D007275:Injections, Intravenous; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008099:Liver / Q000098:blood supply / Q000187:drug effects* / Q000201:enzymology / Q000293:injuries*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D020011:Protective Agents / Q000008:administration & dosage*; D051381:Rats; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism; D013654:Taurine / Q000008:administration & dosage*
chemical_list: D004731:Endotoxins; D020011:Protective Agents; D013654:Taurine; D008315:Malondialdehyde; D007770:L-Lactate Dehydrogenase; D009195:Peroxidase; D053148:Caspase 3