文章摘要
陶〓政,张海鸣,朱秋伟,徐三荣.外源性血管内皮生长因子对大鼠肝缺血再灌注损伤的影响[J].南京医科大学学报,2010,(8):1105~1107
外源性血管内皮生长因子对大鼠肝缺血再灌注损伤的影响
The effect of exogenous vascular endothelial growth factor on hepatic ischemia/reperfusion injury in rats
投稿时间:2010-01-29  
DOI:10.7655
中文关键词: 肝脏  缺血  再灌注损伤  外源性  血管内皮生长因子
英文关键词: liver  ischemia  reperfusion injury  exogenous  vascular endothelial growth factor
基金项目:镇江市社会发展项目(SH2007021)
作者单位
陶〓政 江苏大学附属医院普外科,江苏 镇江〓212001 
张海鸣 江苏大学附属医院普外科,江苏 镇江〓212001 
朱秋伟 江苏大学附属医院普外科,江苏 镇江〓212001 
徐三荣 江苏大学附属医院普外科,江苏 镇江〓212001 
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中文摘要:
      目的:研究外源性血管内皮生长因子(vascular endothelial growth factor,VEGF)对大鼠肝缺血再灌注损伤的影响?方法:雄性SD大鼠30只,体重(300±20)g,随机分为A组(VEGF组)?B组(缺血再灌注组)?C组(手术对照组),其中A?B组建立70%肝缺血再灌注损伤模型?A组于缺血前30 min经腹腔注射VEGF(50 μg/300 g体重);B组于缺血前30 min 经腹腔注射等量生理盐水;C组仅麻醉?开腹,不阻断血流?术后6 h,分别采用全自动生化分析仪?HE染色?ELISA法?比色法分别测定血肝功能酶?肝组织病理改变?肝脏诱导型一氧化氮合成酶(induced nitric oxide synthase,iNOS)活性?肝组织髓过氧化物酶(myeloperoxidase,MPO)的含量?结果:A组应用重组VEGF后血肝功能酶以及肝组织MPO显著低于B组(P < 0.01),肝脏局部iNOS的活性降低,肝组织形态学无明显改变?结论:外源性VEGF能抑制肝脏iNOS的活性,缓解肝功能下降,保护大鼠肝脏缺血再灌注损伤?
英文摘要:
      Objective:To investigate the effects of exogenous vascular endothelial growth factor(VEGF)on hepatic ischemia/reperfusion injury in rats. Methods:Thirty normal male Sprague-Dawley rats were randomly divided into three groups:group A that was subjected to ischemia/reperfusion injury with intraperitoneal administration of VEGF(50 μg/300 g)30 min before ischemia;group B with the same injury followed by saline administration in the same manner,and group C with only anesthetization leparotomy without ischemia. Animals were killed at 6 hours after reperfusion. Routine assays were performed for testing the levels of alanine aminotransferase(ALT),aspartate aminotransferase(AST),lactate dehydrogenase (LDH),the activity of hepatic myeloperoxidase(MPO)and induced nitric oxide synthase (iNOS).The pathological changes in the liver were evaluated in hematoxylin and eosin(HE)stained sections. Results:The levels of serum ALT,AST,LDH and the activity of iNOS,MPO in hepatic tissues increased significantly after hepatic ischemia/reperfusion injury. But these effects were offset by administration of VEGF(P < 0.01). In group B,widespread pathological changes and cell apoptosis were observed in the hepatic tissue following hepatic ischemia/reperfusion injury,while similar changes were scarcely visible in groupe A due to the protective effect of intraperitoneal administration of VEGF 30 min before ischemia. Conclusion:The exogenous VEGF can depress the activity of iNOS and alleviate the liver function during the ischemia/reperfusion period,and protect the liver from ischemia and reperfusion injury.
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