【摘要】：目的研究曲美他嗪對缺氧誘導的心肌細胞凋亡及線粒體能量代謝改變的影響。方法采用胰酶和膠原酶聯(lián)合消化的方法,提取大鼠原代心肌細胞,三氣培養(yǎng)箱模擬缺氧損傷。MTT和Hoechst染色檢測細胞活性和凋亡,TMRE染色檢測線粒體膜電位,Oxygraph-2k細胞呼吸測量儀檢測態(tài)3、態(tài)4呼吸和呼吸控制率,Western blot檢測Caspase-3、細胞色素C以及線粒體呼吸鏈復合酶體Ⅰ、Ⅱ、Ⅲ、Ⅳ、Ⅴ蛋白表達水平的變化。結(jié)果缺氧能夠誘導心肌細胞凋亡、引起線粒體膜電位下降和促進細胞色素C的釋放。此外,缺氧能夠顯著下調(diào)態(tài)3呼吸和上調(diào)態(tài)4呼吸,引起呼吸控制率的下降,同時缺氧能夠不同程度地下調(diào)線粒體呼吸鏈復合酶體Ⅰ、Ⅱ、Ⅲ、Ⅳ、Ⅴ的蛋白表達水平。曲美他嗪能夠顯著降低缺氧誘導的心肌細胞凋亡、穩(wěn)定線粒體膜電位和減少細胞色素C釋放。此外,曲美他嗪還能減輕缺氧對線粒體呼吸鏈復合酶體的損傷,維持線粒體有氧呼吸。結(jié)論曲美他嗪具有抵抗缺氧致心肌細胞凋亡的作用,可能與其穩(wěn)定線粒體膜和呼吸鏈復合酶體有關(guān),繼而減少細胞色素C的釋放和維持線粒體有氧呼吸。
[Abstract]:Aim to study the effects of trimetazidine on hypoxia-induced myocardial apoptosis and mitochondrial energy metabolism. Methods Primary rat cardiomyocytes were extracted by combined digestion of trypsin and collagenase, anoxic injury was simulated in three air incubators, cell activity and apoptosis were detected by MTT and Hoechst staining, mitochondrial membrane potential was detected by TMRE staining. The expression levels of Caspase-3, cytochrome C and mitochondrial respiratory chain complex enzymes 鈪，

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