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Protective effect of prednisolone on ischemia-induced liver injury in rats 被引量:3

Protective effect of prednisolone on ischemia-induced liver injury in rats
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摘要 AIM: To investigate the effects of prednisolone on cell membrane bleb formation, calpain μ activation and talin degradation during hepatic ischemia-reperfusion injury in rats. METHODS: The hilar area of the left lateral and median lobes of rat liver (68%) was clamped for 60 min and followed by 120 min reperfusion. Prednisolone was administered at 1.0, 3.0, or 10 mg/kg at 30 min before ischemia. In addition to biochemical and microscopic analyses, activation of calpain μ was determined using specific antibodies against the intermediate (activated) form of calpain μ. Degradation of talin was also studied by Western blotting. RESULTS: In the control and prednisolone (1.0 mg/kg) groups, serum aspartate transaminase (AST) and alanine transaminase (ALT) level were elevated, and cell membrane bleb formation was observed after 120 min of reperfusion. Moreover, calpain μ activation and talin degradation were detected. Infusion of prednisolone at 3.0 or 10 mg/kg significantly suppressed serum AST and ALT, and prevented cell membrane bleb formation. At 10 mg/kg, prednisolone markedly suppressed calpain μ activation and talin degradation. CONCLUSION: Prednisolone can suppress ischemia- reperfusion injury of the rat liver. Its cytoprotective effect is closely associated with the suppression of calpain μ activation and talin degradation. AIM: To investigate the effects of prednisolone on cell membrane bleb formation, calpain μ activation and talin degradation during hepatic ischemia-reperfusion injury in rats. METHODS: The hilar area of the left lateral and median lobes of rat liver (68%) was clamped for 60 min and followed by 120 min reperfusion. Prednisolone was administered at 1.0, 3.0, or 10 mg/kg at 30 min before ischemia. In addition to biochemical and microscopic analyses, activation of calpain μ was determined using specific antibodies against the intermediate (activated) form of calpain μ. Degradation of talin was also studied by Western blotting. RESULTS: In the control and prednisolone (1.0 mg/kg) groups, serum aspartate transaminase (AST) and alanine transaminase (ALT) level were elevated, and cell membrane bleb formation was observed after 120 min of reperfusion. Moreover, calpain μ activation and talin degradation were detected. Infusion of prednisolone at 3.0 or 10 mg/kg significantly suppressed serum AST and ALT, and prevented cell membrane bleb formation. At 10 mg/kg, prednisolone markedly suppressed calpain μ activation and talin degradation. CONCLUSION: Prednisolone can suppress ischemia- reperfusion injury of the rat liver. Its cytoprotective effect is closely associated with the suppression of calpain μ activation and talin degradation.
出处 《World Journal of Gastroenterology》 SCIE CAS CSCD 2008年第27期4332-4337,共6页 世界胃肠病学杂志(英文版)
关键词 局部缺血-再灌注 波尼松龙 细胞膜泡疹 肝损害 Ischemia-reperfusion Prednisolone Cell membrane bleb Calpain μ Talin
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  • 1[1]Pachter HL,Spencer FC,Hofstetter SR,Coppa GF.Experience with finger fracture technique to achieve intrahepatic hemostasis in 75 patients with severe injuries of liver.Ann Surg 1983; 197:771-778
  • 2[2]Hess ML,Manson NH.The paradox of steroid therapy:inhibition of oxygen free radicals.Circ Shock 1983; 10:1-5
  • 3[3]Liu P,Vonderfecht SL,Fisher MA,McGuire GM,Jaeschke H.Priming of phagocytes for reactive oxygen production during hepatic ischemia-reperfusion potentiates the susceptibility for endotoxin-induced liver injury.Circ Shock 1994; 43:9-17
  • 4[4]Fornander J,Hellman A,Hasselgren PO.Effects of methylprednisolone on protein synthesis and blood flow in the postischemic liver.Circ Shock 1984; 12:287-295
  • 5[5]Glenn TM,Lefer AM.Role of lysosomes in the pathogenesis of splanchnic ischemia shock in cats.Circ Res 1970; 27:783-797
  • 6[6]Nicotera P,HartzeU P,Davis G,Orrenius S.The formation of plasma membrane blebs in hepatocytes exposed to agents that increase cytosolic Ca2+ is mediated by the activation of a non-lysosomal proteolytic system.FEBS Lett 1986; 209:139-144
  • 7[7]Sakaida I,Thomas AP,Farber JL.Increases in cytosolic calcium ion concentration can be dissociated from the killing of cultured hepatocytes by tert-butyl hydroperoxide.J Biol Chem 1991; 266:717-722
  • 8[8]Rosser BG,Gores GJ.Liver cell necrosis:cellular mechanisms and clinical implications.Gastroenterology 1995; 108:252-275
  • 9[9]Gores GJ,Herman B,Lemasters JJ.Plasma membrane bleb formation and rupture:a common feature of hepatocellular injury.Hepatology 1990; 11:690-698
  • 10[10]Miyoshi H,Umeshita K,Sakon M,Imajoh-Ohmi S,Fujitani K,Gotoh M,Oiki E,Kambayashi J,Monden M.Calpain activation in plasma membrane bleb formation during tert-butyl hydroperoxide-induced rat hepatocyte injury.Gastroenterology 1996; 110:1897-1904

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