摘要
目的探讨线粒体通透性转变孔(mPTP)抑制剂环孢素A(CsA)在肺缺血/再灌注损伤(I/R)中的作用以及mPTP作为靶目标肺保护策略的可行性。方法健康家兔40只,随机均分为4组:假手术组、CsA组、低分子右旋糖酐(LMD)组和I/R组。采用原位缺口末端标记(TUNEL)法检测肺组织细胞凋亡情况,免疫组化法检测肺组织细胞色素C(CytC)的含量,电镜下观察肺组织线粒体的破坏情况。结果 CsA组肺组织CytC含量和细胞凋亡指数均高于假手术组(P<0.01),但明显低于LMD组和I/R组,且LMD组的细胞凋亡指数和CytC含量均低于I/R组。结论 CsA能够在再灌注早期抑制mPTP的开放,减少I/R损伤肺组织的细胞凋亡,起到肺保护作用。
Objective To investigate the effects of cyclosporine A( CsA), a inhibitor ot mitochondnal permeability transition pore (mPTP), on lung ischemia/reperfusion (I/R), and explore the viability of lung protection strategy by inhibiting the mPTP. Methods Single lung in vivo I/R animal model was established. 40 rabbits were randomly averagely divided into four groups : sham (S) group, cyclosporine A (CsA) group, low molecular dextran (LMD) and I/R group. Apoptosis of lung tissue pneumocyte was assessed by TUNEL method, Cytochrome C (CytC) in lung tissue was detected by immunohistochemeal techniques, the damage of mitochondrial was observed by electron mi- croscope. Results The content of CytC in cytoplasm and the value of apoptosis index (AI) in CsA group were evi- dently higher than that of S group, but it' s evidently lower than that of LMD group and I/R group, and the value of AI and the content of CytC in LMD group were lower than those of I/R group. Conclusion CsA can inhibit the opening of mPTP in early reperfusion, reduce the apoptosis of lung tissue pneumoeyte, and protect the lung against I/R.
出处
《安徽医科大学学报》
CAS
北大核心
2012年第7期793-796,共4页
Acta Universitatis Medicinalis Anhui
关键词
再灌注损伤
线粒体通透性转变孔
细胞凋亡
环孢素A
reperfusion injury
mitochondrial permeability transition pore
apoptosis
cyclosporine A