ALDH2通过调控线粒体网络减轻心肌缺血-再灌注损伤
首发时间:2017-04-27
摘要:乙醛脱氢酶2(ALDH2)是位于线粒体基质内的酶,具有重要的心肌保护作用。心肌缺血-再灌注过程中线粒体分裂增加形成大量片段化线粒体,而抑制线粒体分裂则减少细胞死亡。为了研究ALDH2是否通过调控线粒体融合分裂发挥心肌保护作用,我们选用大鼠心肌细胞H9C2作为细胞模型,在缺氧-复氧培养条件下,给予ALDH2激活剂Alda-1处理;在荧光显微镜下观察线粒体的形态变化;并观察细胞凋亡情况。本实验发现使用Alda-1激活ALDH2活性后,显著降低缺氧-复氧条件下的线粒体分裂,减少细胞凋亡。表明ALDH2可能通过调控线粒体网络对细胞凋亡发挥调节作用。
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ALDH2 reduces myocardial ischemia-reperfusion injury by regulating mitochondrial fusion and fission
Abstract:ALDH2 (Acetaldehyde dehydrogenase 2) which located in mitochondrial matrix, plays a myocardiac protective role in hypoxia-reoxygennation. Mitochondrial fission increases after hypoxia-reoxygennation, and inhibiting mitochonrial fission could attenuate cell death. Here, we emphasize to explore the roles of ALDH2 in the morphology of mitochondria. After incubating H9C2 cells with ALDH2 activator Alda-1, we detect the effect of ALDH2 on the morphology of mitochondria after hypoxia-reoxygennation through fluorescence microscope and detect the cell apoptosis. We found that the use of Alda-1 in H9C2 cells could decrease mitochondial fission and cell apoptosis after hypoxia-reoxygennation. These results indicating the important roles of ALDH2 in the maintenance of mitochondrial morphology.
Keywords: ALDH2 hypoxia-reoxygennation mitochondria fission apoptosis
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No.4728277119544714****
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