四川大学学报（医学版）2012，Vol.43Issue(4)：483-487,5.
丙烯醛对缺氧复氧H9c2心肌细胞损伤的影响及机制初探
Effects of Acrolein on Apoptosis of H9c2 Cardiacmyocytes with Hypoxia/Reoxygenation Injury
摘要
Abstract
Objective To determine the cytotoxic effects of acrolein on hypoxia/ reoxygenation (H/R) injury in H9c2 cardiacmyocytes and investigate the intracellular signaling pathways. Methods Hypoxia/reoxygenation (H/R) injury model was established with H9c2 cells. The H9c2 cells were divided into four groups, the control group, acrolein group (ACR), H/R group, acrolein+ H/R group (ACR+ H/R). H9cZ cells pretreated with or without acrolein (10 μmol/L) for 30 min were exposed to 2 h hypoxia and 16 h reoxygenation. The effect of acrolein on the cellular viability and apoptosis of H9c2 cells was measured by MTT assay, DAPI stainning and flow cytometry (FCM) respectively. The expression of apotosis-related proteins (cytochrome c, caspase 9 and caspase 3) in the H9c2 cells was detected by Western blot. Results Compared with mere H/R treatment, the decrease in cell viability and increase in the number of apoptotic cells in H9c2 cells subjected to H/R were significantly exacerbated in the presence of acrolein (P<0. 05). The liberation of cytochrome c from mitochondria to cytosol, the cleavages of the initiator caspase 9 and the effector caspase 3 have been observed after pretreatment with acrolein followed by H/ R in H9c2 cells. Conclusion Acrolein could aggravate H/R injury and that this effect may be related, in part, to the modification of proteins involved the release of cytochrome c from mitochondria to cytosol and activation of caspases cascade reaction.关键词
丙烯醛/H9c2心肌细胞/缺氧复氧/凋亡/线粒体Key words
Acrolein/H9c2 cardiacmyocytes/Hypoxia/reoxygenation/Apoptosis Mitochondria引用本文复制引用
邵庆瑞,杜丹,何阳,吴晓华,黄文,邢志华..丙烯醛对缺氧复氧H9c2心肌细胞损伤的影响及机制初探[J].四川大学学报（医学版）,2012,43(4):483-487,5.基金项目
国家"12.5"基金(No.2011BAJ07B04)、国家自然科学基金(No.20972105)和四川省基金会(No.2008SZ0024)资助 （No.2011BAJ07B04）
