摘要
目的探讨高浓度氧暴露后对新生大鼠肺组织细胞色素C(CytC)、caspase-3动态表达及细胞凋亡的影响。方法将48例新生Spraque-Dawley大鼠生后立即随机分为空气组、高氧组,高氧组予以≥95%氧浓度持续暴露。两组分别于高氧或空气暴露后1、2、3、4 d应用脱氧核糖核酸转移酶介导的细胞凋亡标记技术检测细胞凋亡,Western blot检测胞质和线粒体内CytC蛋白含量,免疫组织化学检测caspase-3蛋白分布及含量。结果与空气组相比,高氧组肺组织细胞凋亡指数第3天开始持续升高(P<0.01);与空气组相比,高氧暴露2 d胞质内CytC蛋白水平开始增加(P<0.05),3 d达到高峰;线粒体内CytC蛋白水平于第2天开始持续下降(P<0.05);caspase-3蛋白水平于高氧暴露3 d开始增加,呈上升趋势(P<0.05)。结论高氧暴露可致新生大鼠肺组织CytC蛋白由线粒体释放至胞质,CytC分布发生变化,可能通过激活caspase-3进而导致线粒体途径介导的细胞凋亡,从而引起高氧肺损伤。
Objective To investigate the influence of hyperoxia on cytochrome c,caspase-3 expression and apoptosis in the lungs of neonatal rats.Methods 48 neonatal Sprague-Dawley rats were randomly divided into two groups：air group and hyperoxia group.The neonatal rats in hyperoxic group were exposed to ≥95% oxygen after birth to establish hyperoxic lung injury model,while air group were in room air.The rats were sacrificed 1,2,3 and 4 days after air or hyperoxia exposure.Lung cell apoptosis were observed by TUNEL assay.The levels of CytC protein in cytoplasm and mitochondria were detected by Western blot.The distribution and content of caspase-3 protein was detected by immunohistochemistry.Results Compared with the air group,the apoptosis index of lung tissue in the hyperoxia group kept rising from the third day（P0.01）Compared with the air group,cytoplasmal CytC protein levels in hyperoxia group began to increase on the second day（P0.05）,and reach peak on the third day;mitochondrial CytC protein levels began to decline on the second day（P0.05）;caspase-3 protein levels in hyperoxia group began to increase in the third day,and remain rising（P0.05）.Conclusion Exposure to hyperoxia during neonatal period can result in releasing of CytC from mitochondria to cytoplasm and changing of CytC distribution,possibly through activation of caspase-3 leading to mitochondrial pathway-mediated apoptosis,resulting in hyperoxic lung injury.
出处
《医学综述》
2011年第13期2053-2055,共3页
Medical Recapitulate
