BH3-only蛋白（bcl-2 homology domain only proteins）是Bcl-2蛋白家族中启动和调节细胞凋亡的重要成员，能识别不同的细胞刺激形式并被活化，其活性受转录和／或翻译后修饰的调节。BH3-only蛋白通过抑制Bcl-2抗凋亡成员的活性或激活Ba...BH3-only蛋白（bcl-2 homology domain only proteins）是Bcl-2蛋白家族中启动和调节细胞凋亡的重要成员，能识别不同的细胞刺激形式并被活化，其活性受转录和／或翻译后修饰的调节。BH3-only蛋白通过抑制Bcl-2抗凋亡成员的活性或激活Bax／Bak样促凋亡成员的活性来调节细胞凋亡，在组织发育、维持内环境稳定、防止自身免疫病和肿瘤的发生中有着极其重要的作用。本文主要就BH3-only蛋白对凋亡的调控研究作一综述。展开更多
Objectives To investigate the effect of co-exposure of myocardial ischemia and cold stress on myocardial injury in rats and the relative mechanism.Methods Myocardial ischemia model was established by ligation of left ...Objectives To investigate the effect of co-exposure of myocardial ischemia and cold stress on myocardial injury in rats and the relative mechanism.Methods Myocardial ischemia model was established by ligation of left coronary artery.SD rats were randomly allocated to 4 groups; sham+normal temperature(S group),sham+cold stress(SC group),myocardial ischemia+ normal temperature(Ⅰgroup), myocardial ischemia+cold stress(IC group).On the condition of 26℃,SC and IC groups were keeped in a 4℃artificial chamber for 8h(8;00-16:00) for 4 consecu- tive days.Car diac function was assessed by echocardiography;pathological change was analyzed by HE staining;myocardial infarct size was determined by TTC staining;Bim,Caspase-3 expression in myocardium was determined by western blotting.Results It was demonstrated that co-exposure of myocardial ischemia and cold stress could significantly make the cardiac muscle in abnormal shape,increase the infarct size and the expression of Bim and Caspase-3.Conclusions Co-exposure of myocardial ischemia and cold stress may aggravate the cardiac injury,pro- apoptosis protein Bim is involved.展开更多
文摘BH3-only蛋白（bcl-2 homology domain only proteins）是Bcl-2蛋白家族中启动和调节细胞凋亡的重要成员，能识别不同的细胞刺激形式并被活化，其活性受转录和／或翻译后修饰的调节。BH3-only蛋白通过抑制Bcl-2抗凋亡成员的活性或激活Bax／Bak样促凋亡成员的活性来调节细胞凋亡，在组织发育、维持内环境稳定、防止自身免疫病和肿瘤的发生中有着极其重要的作用。本文主要就BH3-only蛋白对凋亡的调控研究作一综述。
文摘Objectives To investigate the effect of co-exposure of myocardial ischemia and cold stress on myocardial injury in rats and the relative mechanism.Methods Myocardial ischemia model was established by ligation of left coronary artery.SD rats were randomly allocated to 4 groups; sham+normal temperature(S group),sham+cold stress(SC group),myocardial ischemia+ normal temperature(Ⅰgroup), myocardial ischemia+cold stress(IC group).On the condition of 26℃,SC and IC groups were keeped in a 4℃artificial chamber for 8h(8;00-16:00) for 4 consecu- tive days.Car diac function was assessed by echocardiography;pathological change was analyzed by HE staining;myocardial infarct size was determined by TTC staining;Bim,Caspase-3 expression in myocardium was determined by western blotting.Results It was demonstrated that co-exposure of myocardial ischemia and cold stress could significantly make the cardiac muscle in abnormal shape,increase the infarct size and the expression of Bim and Caspase-3.Conclusions Co-exposure of myocardial ischemia and cold stress may aggravate the cardiac injury,pro- apoptosis protein Bim is involved.
