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目的探讨凋亡相关因子Bax、Bcl-2、细胞色素C和caspase-3在缺氧缺水缺食条件下大鼠心肌细胞损伤中变化及其意义。方法将80只Wistar大鼠置于常压低氧舱(10%氧浓度)并禁食水,于实验1、3、5、7 d,采用原位末端标记、免疫组织化学和原位杂交技术等方法,检测缺氧缺水缺食后心脏凋亡指数变化及凋亡相关因子Bax、Bcl-2、细胞色素C和caspase-3在其中的作用。结果 10%缺氧复合缺水缺食后1 d和7 d大鼠心肌细胞凋亡指数(62.63±14.97)、(20.19±3.26)增加;Bax、细胞色素C和caspase-3蛋白在单纯缺氧和缺氧缺水缺食后均可见1~7 d表达增加,缺水缺食后在3~7 d表达增加。Bcl-2在单纯缺氧和缺水缺食后1~7 d表达减少,缺氧缺水缺食后1~3 d表达减少;Caspase-3 mRNA在单纯缺氧组和缺氧缺水缺食后1 d(4.19±1.42)、(3.87±0.86)和7 d(10.43±2.79)、(12.12±2.27)表达增加,缺水缺食后1 d(3.85±0.88)表达增加。结论 10%缺氧复合缺水缺食可引起心肌细胞凋亡,与Bax表达增加、Bcl-2表达减少有关;可能进一步通过线粒体途径,释放细胞色素C,激活caspase-3,引发心肌细胞凋亡。
Objective To investigate the changes and significance of apoptosis-related factors Bax, Bcl-2, cytochrome C and caspase-3 in cardiomyocyte injury induced by hypoxia and water deficit in rats. Methods 80 Wistar rats were placed in normobaric hypoxia chamber (10% oxygen concentration) and fasted water for 1, 3, 5 and 7 days. End-stage end labeling, immunohistochemistry and in situ hybridization And other methods to detect changes in cardiac apoptotic index and apoptosis-related factors Bax, Bcl-2, cytochrome C and caspase-3 in hypoxia and water deficiency. Results Apoptotic index (62.63 ± 14.97) and (20.19 ± 3.26) of rats in 10% hypoxia combined with water scarcity were significantly increased at 1 d and 7 d, respectively. Bax, cytochrome C and caspase- And hypoxia and water deficiency can be seen after 1 to 7 d expression increased, lack of water after 3 to 7 d increased expression. The expression of Bcl-2 decreased from 1 to 7 days after hypoxia and lack of water, and decreased 1 to 3 days after hypoxia and water lack. The expression of Caspase-3 mRNA in hypoxia and water deficient (4.19 ± 1.42), (3.87 ± 0.86), and 7d (10.43 ± 2.79), (12.12 ± 2.27) on the 1st day, and increased on the 1st day after scanty watering (3.85 ± 0.88). Conclusions 10% hypoxia combined with lack of water can induce cardiomyocyte apoptosis, which is related to the increase of Bax expression and the decrease of Bcl-2 expression. It may further release mitochondrial cytochrome C and activate caspase-3 to induce cardiomyocyte apoptosis .