文章摘要
王继萍,冬 冬,童 岚,冷吉燕.rhKD/APP对大鼠肝脏缺血再灌注损伤的保护作用及其机制的研究[J].南京医科大学学报,2008,28(7):885~888
rhKD/APP对大鼠肝脏缺血再灌注损伤的保护作用及其机制的研究
The protective effect and mechanism of rhKD/APP on liver ischemia-reperfusion injury of rats
投稿时间:2008-01-12  
DOI:10.7655
中文关键词: rhKD/APP  肝损伤  缺血再灌注损伤
英文关键词: rhKD/APP  hepatic cell  ischemia-reperfusion injury
基金项目:
作者单位
王继萍 吉林大学第一医院放射科,吉林 长春 130021 
冬 冬 吉林大学第一医院放射科,吉林 长春 130021 
童 岚 吉林大学第一医院放射科,吉林 长春 130021 
冷吉燕 吉林大学第一医院干部病房,吉林 长春 130021 
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中文摘要:
      目的:探讨人Kunitz型蛋白酶抑制剂(rhKD/APP)对大鼠肝脏缺血再灌注损伤的保护作用及机制?方法:将60只大鼠随机分为6组即假手术组(空白组)?模型组?rhKD/APP小剂量组?中剂量组?大剂量组?对照药物抑肽酶组,每组10只?制成部分肝脏缺血再灌注模型,缺血40 min后再灌注3 h,摘眼球取血处死大鼠并取肝组织,进行血清丙氨酸转氨酶(ALT)?天冬氨酸转氨酶(AST)?碱性磷酸酶(ALP)活性测定?制做肝组织切片进行光镜及电镜观察?免疫组化方法测定肝组织内TNF-α蛋白的表达?结果:rhKD/APP小?中?大剂量组与模型组比较, 均可以不同程度降低肝损伤大鼠血清ALT?AST?ALP活性(P < 0.01)?从组织病理形态学及超微结构方面可见,rhKD/APP小?中?大剂量组可以在不同程度上减轻肝损伤?各个剂量 rhKD/APP组可以抑制TNF-α蛋白的表达(P < 0.01)?结论:rhKD/APP对大鼠缺血再灌注肝损伤具有显著保护作用,抑制参与炎性反应的TNF-α是其机制之一?
英文摘要:
      Objective:To investigate the protective effect of rhKD/APP on liver ischemia-reperfusion injury of rats and its mechanism. Methods:All rats were divided into 6 groups randomly, sham-operation group, model group, rhKD/APP treatment groups and Aprotinin group, 10 in each group. rhKD/APP was given with different dose in rhKD/APP treatment groups. Pathological model of liver ischemia-reperfusion injury of rats was set up. Rats were killed after 40 min ischemia and 3 h reperfusion. The levels of ALT, AST and ALP in serum were measured. Hepatic tissue was observed under light and electronic microscopy. The expression of TNF-α protein in tissue was determined by immunohistochemistry. Results:rhKD/APP can significantly decrease the activities of ALT, AST and ALP. Under light and electronic microscopy, the extent of damaged hepatic tissue were observed decreased in the groups treated with rhKD/APP. Expression of TNF-α protein in tissue was significantly reduced(P < 0.01). Conclusion:rhKD/APP has a protective effect on liver ischemia-reperfusion injury of rats. rhKD/APP can obviously inhibit the inflammatory process by inhibiting TNF-α.
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