摘要
目的:从Bcl-xl/s基因和蛋白水平探讨缺血后处理抗大鼠心肌细胞凋亡的机制。方法:18只健康Wistar大鼠随机分为假手术(Sham)组、缺血再灌注损伤(I/R)组、缺血后处理(PostC)组,每组6只。采用原位缺口末端标记(TUNEL)检测大鼠心肌细胞凋亡指数;免疫组化法检测BcL-xl/s蛋白表达水平;荧光实时定量PCR法检测心肌组织Bcl-xl/s基因表达水平。结果:与I/R组相比,PostC组再灌注后心肌细胞凋亡指数明显降低,PostC组Bcl-xl蛋白及mRNA表达水平明显上调,Bcl-xs蛋白及mRNA表达水平明显下调。结论:PostC能显著减少缺血再灌注后心肌细胞凋亡,凋亡相关基因Bcl-xl、Bcl-xsmRNA及蛋白参与了由缺血再灌注诱导的心肌细胞凋亡。
Objective：To study the mechanism of anti-apoptosis and changed expression of Bcl-xl/s in ischemic postconditioning （PostC） in rats. Methods： Eighteen healthy adult male Wistar rats were divided into three groups including Sham group, ischemia-reperfusion （I/R） group and PostC group （n=6 for each）. TUNEL staining was used to analyse the myocardial apoptotic index. Immunohistochemisty was used to detect the protein level of Bcl-xl/s. The expressions of Bcl-xl mRNA and Bcl-xs mRNA were determined by real-time PCR. Results： Compared with I/R group, the cardiomyocyte apoptotic index significantly decreased, the expression of Bcl-xl protein and Bcl-xl mRNA increased in PostC group. The expressions of Bcl-xs protein and Bcl-xs mRNA decreased significantly in PostC group than those of I/R group. Conclusion： PostC can significantly decrease the cardiomyocyte apoptosis after I/R injury, in which Bcl-xl and Bcl-xs mRNA involved in I/R-induced myocardial apoptosis.
出处
《天津医药》
CAS
北大核心
2011年第12期1130-1132,I0010,共4页
Tianjin Medical Journal
基金
国家自然科学基金资助项目(项目编号:81041042)
天津市应用基础及前沿技术研究计划项目(项目编号:10JCZDJC19200)
天津医科大学科学基金资助项目(项目编号:2009KY30)
