论文部分内容阅读
目的:探讨CD38基因缺失对小鼠心肌缺血再灌注损伤的保护作用及其机制。方法:利用CD38基因敲除及野生型小鼠进行在体小鼠心脏左前降支结扎,缺血30 min后复灌24 h取心脏,1 mm切片进行TTC染色确定其梗死面积差异。利用shRNA干扰系统构建的CD38稳定干扰H9c2细胞系模拟体外缺氧复氧损伤。用CCK-8法确定最佳缺氧复氧损伤时间,再利用流式细胞术对缺氧复氧后氧化应激诱导的活性氧含量进行检测,利用Hoechst 33258染色法检测损伤诱导的细胞凋亡。分离提取
Objective: To investigate the protective effect of CD38 gene deletion on myocardial ischemia-reperfusion injury in mice and its mechanism. Methods: CD38 knockout and wild-type mice were ligated in the left anterior descending branch of the heart of a mouse. The hearts were revulled for 30 min after reperfusion and the infarct size was determined by TTC staining in 1 mm sections. CD38 Stable Interfering with shRNA Interference System H9c2 cell line mimics in vitro hypoxia - reoxygenation injury. The best hypoxia-reoxygenation injury time was determined by CCK-8 method, and the oxidative stress-induced reactive oxygen species (ROS) levels were detected by flow cytometry. The damage induced by injury was detected by Hoechst 33258 staining . Separation and extraction