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血红素加氧酶-1诱导对鼠肝缺血再灌注损伤的保护作用
引用本文:黄秀芳,陈必成,胡正杨,林丽娜,罗爱林.血红素加氧酶-1诱导对鼠肝缺血再灌注损伤的保护作用[J].肝胆胰外科杂志,2006,18(2):95-96.
作者姓名:黄秀芳  陈必成  胡正杨  林丽娜  罗爱林
作者单位:1. 温州医学院第一附属医院,麻醉科,浙江,温州,325000
2. 华中科技大学同济医学院同济医院,武汉,430030
3. 华中科技大学同济医学院同济医院,麻醉科,武汉,430030
摘    要:目的研究血红素加氧酶-1(heme oxygenase-1,HO-1)在鼠肝缺血再灌注损伤肝组织中的表达及其作用。方法建立小鼠部分肝脏热缺血再灌注损伤模型,36只清洁级Balb/C小鼠随机分为3组: 假手术组(S组)、缺血/再灌注损伤组(I/R组)、HO-1诱导剂氯化高铁血红素(hemin)预处理组(HM组)。免疫组化半定量分析肝组织HO-1蛋白的表达,检测血清AST和ALT,肝组织丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性,并观察肝组织的病理变化。结果与S组比较,I/R组HO-1蛋白表达显著增强,hemin预处理后,HO-1蛋白表达较I/R组增高(P<0.01)。I/R组AST,ALT活性和MDA的含量显著高于S组,而HM组均显著低于I/R组(P<0.01);I/R组SOD活性下降,而HM组显著高于I/R组(P<0.01)。HM组病理损伤程度明显轻于I/R组。结论 HO-1在鼠肝缺血再灌注损伤肝组织中表达上调,对肝脏具有保护效应。

关 键 词:血红素加氧酶-1  肝缺血  再灌注损伤  氯化高铁血红素
文章编号:1007-1954(2006)01-0095-02
修稿时间:2005年12月12

Protective role of heme oxygenase-1 on the liver ischemia/reperfusion injury
HUANG Xiu-fang,CHEN Bi-cheng,HU Zheng-yang,et al..Protective role of heme oxygenase-1 on the liver ischemia/reperfusion injury[J].Journal of Hepatopancreatobiliary Surgery,2006,18(2):95-96.
Authors:HUANG Xiu-fang  CHEN Bi-cheng  HU Zheng-yang  
Institution:HUANG Xiu-fang,CHEN Bi-cheng,HU Zheng-yang,et al. Department of Anesthesiology,First Affiliated Hospital,Wenzhou Medical College,Wenzhou 325000
Abstract:Objective To investigate the protein expression of heme oxygenase-1(HO-1) after liver ischemia/reperfusion(I/R) and its influences. Methods The model of partial hepatic ischemia were established in Balb/C mice. 36 mice were divided at random into sham-operation group(S), liver ischemia/reperfusion group (I/R), and induce of HO-1(hemin) pretreatment group (HM). The protein expression of HO-1 was observed using immunohistochemical technique and assessed semi-quantitatively. The activity of serum aspartate transaminase (AST) and alanine transaminase(ALT) were assessed. The liver malondialdehyde(MDA) content, SOD activity and liver histpathological changes were detected respectively. Results Compared with that in S group, the expression of HO-1 was significantly increased in I/R group(p<0.01). In I/R group, the liver enzymes and MDA content were obviously higher than those in S group (p<0.01), but they were decreased obviously when pretreated with hemin. the SOD activity were significantly increased in I/R group, but redued in HM group. Under microscope, the histopathologic results revealed that the injury in HM group was mild compared with that in I/R group. Conclusion The HO-1 protein induced by hemin pretreatment may contribute to the protection on liver I/R injury.
Keywords:heme oxygenase-1  liver ischemia  reperfusion injury  hemin
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