摘要
目的:探讨整体低氧预处理(HPC)对肺缺血-再灌注损伤(I/R)的保护效应。方法:重复低氧5次,建立大鼠HPC模型,用无创微血管夹夹闭左侧肺门45min,1h后松开再灌注180min建立肺I/R模型;设立假手术组、肺I/R组、HPC+肺I/R组,HE染色观察各组肺组织病理学改变,称重计算各组肺湿重与干重比值,免疫组织化学染色方法检测肺组织内细胞色素C的表达,TUNEL法检测肺细胞凋亡。结果:与假手术组相比,肺I/R组肺组织病理学改变明显,肺组织湿/干重比、肺组织细胞色素C表达及凋亡指数显著增高(P<0.05);与肺I/R组比较,HPC+肺I/R组肺组织病理学改变明显改善,其余各检测指标均降低(P<0.05)。结论:大鼠整体低氧预处理可减少肺组织细胞线粒体释放细胞色素C,抑制细胞凋亡从而保护肺I/R损伤。
Objective： To investigate the protective effect of whole-body hypoxic preconditioning （HPC） on ischemia/reperfusion（lung-I/R） caused lung injury in rats. Methods： HPC model rat was established with repetitive sublethal hypoxia for 5 times, while lung-I/R rat was prepared with left lung hilar clamping for 45 min followed by 180-min reperfusion. Thirty rats were randomly divided into 3 groups （n = 10, respectively）： sham-operation group （group S）, lung-I/R group （group I/R） and HPC ＋ lung-I/R group （group H）. After the experiment, lung weights were measured and wet/dry ratioes were calculated, lung morphological changes were observed on HE stained sections, expression of cytochrome C was detected with immunohistochemitry method, and cell apoptosis was assessed with TUNEL method. Result： Compared with those in group S, pathological changes of lung tissue were more obvious, and wet/dry ratio, cytochrome C expression, and cell apoptosis index were significantly increased（P 〈 0.05）in group I/R; While in group H, lung tissue pathological chages were milder, and the other indexes were markedly lowered than those in group I/R. Conclusion： Whole-body hypoxic preconditioning in rats can protect lung from I/R caused injury by reducing release of cytochrome C and inhibiting cell apoptosis.
出处
《贵阳医学院学报》
CAS
2009年第5期504-507,共4页
Journal of Guiyang Medical College
基金
贵州省省长基金资助项目(S2003-9)
