Bcl-2及Bax在心肌损伤中的表达及意义研究

发布时间：2018-06-23 16:04

本文选题：心肌细胞 + Bcl-2　；参考：《吉林大学》2007年硕士论文

【摘要】： 细胞凋亡是近几年来较为热门的课题,在多种疾病的发生、发展过程中具有重要的意义。Bcl-2基因蛋白家族在细胞凋亡的调控中发挥着重要的作用。Bcl-2被认为是细胞凋亡调控的最后通路之一。而Bax作为Bcl-2的同源体,其作用是抑制Bcl-2作用,其与Bcl-2基因一样在组织广泛表达。Bax与Bcl-2在细胞中的比例决定细胞是否发生凋亡。Bax过量时,形成Bax-Bax同二聚体,诱导细胞凋亡;Bcl-2过量时,形成Bcl-2-Bax异二聚体,抑制细胞凋亡。本研究对Wistar大鼠采用分5点一次性皮下注射盐酸异丙基肾上腺素的方法复制心肌缺血缺氧性坏死模型,并分别于注射12 h、1 w和3 w时,用免疫组化方法、RT-PCR法检测各组大鼠心肌组织中Bcl-2、Bax的表达情况,以探讨Bcl-2、Bax在异丙基肾上腺素所致心肌损伤中与心肌细胞凋亡及心肌纤维化的关系。得出主要结论如下:①Isp可诱导心肌细胞凋亡,并主要通过此途径导致心肌细胞死亡。②Isp诱导心肌细胞凋亡的机制与Bax大量表达,Bax/Bcl-2比例异常增高有关。③心肌细胞在Isp作用下,激活Bax基因,大量表达Bax,同时,抑凋亡基因Bcl-2表达减少,启动心肌细胞凋亡机制,从而发生心肌细胞凋亡;大量凋亡细胞的集中出现表现为点状坏死。④心肌细胞的凋亡是心肌纤维化的诱因,最终导致心肌纤维化的发生。
[Abstract]:Apoptosis is a hot topic in recent years, in the occurrence of many diseases, Bcl-2 gene family plays an important role in the regulation of apoptosis. Bcl-2 is considered to be one of the final pathways of apoptosis regulation. Bax, as a homologue of Bcl-2, inhibits Bcl-2. The ratio of Bax and Bcl-2 in cells determines whether or not apoptosis. Bax is the same dimer as Bcl-2 gene. Bcl-2-Bax heterodimer was formed when apoptosis was induced in excess of Bcl-2, and apoptosis was inhibited. In this study, Wistar rats were injected subcutaneously with isoproterenol hydrochloride for 5 points to establish myocardial ischemic hypoxic necrosis model, and the rats were injected for 12 hours for 1 week and 3 weeks, respectively. Immunohistochemical method was used to detect the expression of Bcl-2P Bax in myocardial tissue of rats in each group, and to investigate the relationship between Bcl-2 Bax and myocardial cell apoptosis and myocardial fibrosis in isoproterenol induced myocardial injury. The main conclusions are as follows: 1 isp can induce cardiomyocyte apoptosis. The mechanism of cardiomyocyte apoptosis induced by 2Isp through this pathway is related to the abnormal ratio of Bax and Bax / Bax / Bax / Bax / Bax / Bax / Bax / Bx / Bcl-2, which is related to the activation of Bax gene and the expression of Baxgene in cardiomyocytes under the action of Isp. At the same time, The expression of anti-apoptosis gene Bcl-2 was decreased, the mechanism of cardiomyocyte apoptosis was initiated, and the concentration of a large number of apoptotic cells showed that the apoptosis of cardiac myocytes was the inducement of myocardial fibrosis. Eventually leading to myocardial fibrosis.
【学位授予单位】：吉林大学
【学位级别】：硕士
【学位授予年份】：2007
【分类号】：R363.2

【引证文献】