本文選題：心肌細(xì)胞 + Bcl-2　； 參考：《吉林大學(xué)》2007年碩士論文

【摘要】： 細(xì)胞凋亡是近幾年來(lái)較為熱門的課題,在多種疾病的發(fā)生、發(fā)展過(guò)程中具有重要的意義。Bcl-2基因蛋白家族在細(xì)胞凋亡的調(diào)控中發(fā)揮著重要的作用。Bcl-2被認(rèn)為是細(xì)胞凋亡調(diào)控的最后通路之一。而B(niǎo)ax作為Bcl-2的同源體,其作用是抑制Bcl-2作用,其與Bcl-2基因一樣在組織廣泛表達(dá)。Bax與Bcl-2在細(xì)胞中的比例決定細(xì)胞是否發(fā)生凋亡。Bax過(guò)量時(shí),形成Bax-Bax同二聚體,誘導(dǎo)細(xì)胞凋亡;Bcl-2過(guò)量時(shí),形成Bcl-2-Bax異二聚體,抑制細(xì)胞凋亡。 本研究對(duì)Wistar大鼠采用分5點(diǎn)一次性皮下注射鹽酸異丙基腎上腺素的方法復(fù)制心肌缺血缺氧性壞死模型,并分別于注射12 h、1 w和3 w時(shí),用免疫組化方法、RT-PCR法檢測(cè)各組大鼠心肌組織中Bcl-2、Bax的表達(dá)情況,以探討B(tài)cl-2、Bax在異丙基腎上腺素所致心肌損傷中與心肌細(xì)胞凋亡及心肌纖維化的關(guān)系。得出主要結(jié)論如下:①Isp可誘導(dǎo)心肌細(xì)胞凋亡,并主要通過(guò)此途徑導(dǎo)致心肌細(xì)胞死亡。②Isp誘導(dǎo)心肌細(xì)胞凋亡的機(jī)制與Bax大量表達(dá),Bax/Bcl-2比例異常增高有關(guān)。③心肌細(xì)胞在Isp作用下,激活Bax基因,大量表達(dá)Bax,同時(shí),抑凋亡基因Bcl-2表達(dá)減少,啟動(dòng)心肌細(xì)胞凋亡機(jī)制,從而發(fā)生心肌細(xì)胞凋亡;大量凋亡細(xì)胞的集中出現(xiàn)表現(xiàn)為點(diǎn)狀壞死。④心肌細(xì)胞的凋亡是心肌纖維化的誘因,最終導(dǎo)致心肌纖維化的發(fā)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.
【學(xué)位授予單位】：吉林大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2007
【分類號(hào)】：R363.2

【引證文獻(xiàn)】

相關(guān)博士學(xué)位論文 前1條

1 徐惠梅;心寧丸抗心肌缺血大鼠的實(shí)驗(yàn)研究[D];黑龍江中醫(yī)藥大學(xué);2010年

相關(guān)碩士學(xué)位論文 前1條

1 張啟霞;TIMP-1在大鼠心肌纖維化中的作用及與細(xì)胞凋亡的關(guān)系[D];吉林大學(xué);2010年

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本文編號(hào)：2057680