血红素加氧酶-1在肺早期缺血再灌注损伤中的表达及意义  

Significance of Heme Oxygenase-1 Expression in Lung Early Ischemia/Reperfusion Injury

作　　者：江科[1] 王建军[1] 李劲松[1] 刘全[1] 杨光海[1] 

机构地区：[1]华中科技大学同济医学院附属协和医院胸外科,武汉430022

出　　处：《华中科技大学学报（医学版）》2007年第4期475-477,481,共4页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong

摘　　要：目的研究血红素加氧酶-1(HO-1)与供肺缺血再灌注损伤之间的关系。方法采用改进的套管吻合技术,建立同系大鼠左肺原位再灌注损伤的动物模型。采用HO-1的诱导剂钴原卟啉(CoPP)和抑制剂锌原卟啉(ZnPP)分别进行干预处理后,运用免疫组织化学技术和RT-PCR技术分别检测HO-1蛋白在供肺组织中的表达以及供肺中HO-1mRNA的表达;运用TUNEL技术检测供肺组织中细胞凋亡。结果肺组织发生缺血再灌注时可诱导HO-1蛋白的表达,且随着再灌注时间的延长,表达逐步增多,再灌注8 h后达到高峰;再灌注前使用CoPP进行预处理,可以诱导HO-1蛋白的表达上调。HO-1蛋白表达上调可以降低肺缺血再灌注后细胞凋亡的发生率。结论肺缺血再灌注损伤可诱导HO-1表达上调,CoPP诱导的HO-1过表达可以抑制肺缺血再灌注损伤诱导的肺细胞凋亡,从而减轻供肺的再灌注损伤。Objective To investigate the expression and significance of heme oxygenase-1 （HO-1） in lung ischemia/reperfusion injury. Methods By using modified cuff anastomosis technique, syngeneic rat orthotopic lung reperfusion injury model was established. The expression of HO-1 mRNA and protein was detected by using RT-PCR and immunohistochemistry respectively in donor lung ischemia/reperfusion tissues treated with Cobalt protoporphyrin （HO-1 inducer） or Zinc protoporphyrin （HO-1 inhibitor）. In situ TUNEL was used to assay the apoptosis in lung tissue. Results The HO-1 expression could be induced by lung ischemia/reperfusion, increased with the time of reperfusion, and reached the peak at 8 h after reperfusion. Pretreatment of CoPP before reperfusion could up-regulate the expression of HO-1, subsequently reduce the incidence of apoptosis after lung reperfusion. Conclusion Lung isehemia/reperfusion injury can induce the up-regulation of HO-1 expression, which can inhibit the-apoptosis of the lung cells and subsequently alleviate the donor lung ischemia/reperfusion injury.

关 键 词：肺缺血再灌注损伤 细胞凋亡 血红素加氧酶-1 

分 类 号：R655.3[医药卫生—外科学]