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目的:采用X染色体连锁凋亡抑制蛋白(XIAP)对缺氧-复氧诱导心肌细胞凋亡模型进行干预,以探讨脂质体介导XIAP基因转染对缺氧-复氧诱导的新生大鼠心肌细胞凋亡的影响。方法:体外培养新生大鼠心肌细胞,分为4组,①XIAP组:将pDsRed2-XIAP以脂质体转染到心肌细胞48h后进行缺氧2h-复氧1h;②预处理组:先将心肌细胞进行缺氧预处理,然后进行缺氧2h-复氧1h;③单纯缺氧-复氧组:将心肌细胞直接进行缺氧2h-复氧1h;④常氧组:将心肌细胞在CO2孵箱中培养3h。各组最后用流式细胞仪Annexin V FITC检测心肌细胞凋亡率结果组间差异。结果:①pDsRed2-XIAP可以通过脂质体转染的方式转染到心肌细胞;②与单纯缺氧-复氧组比较,XIAP组和预处理组心肌细胞凋亡率明显减低,P<0.01;③XIAP组与预处理组比较二者心肌细胞凋亡率相似,P>0.05。结论:以物理性的缺氧2h-复氧1h的方式能诱导所培养的心肌细胞发生凋亡;XIAP能明显减少缺氧-复氧诱导新生大鼠心肌细胞的凋亡;XIAP抑制凋亡的效应与缺氧预处理抑制凋亡的效应相似。
OBJECTIVE: To investigate the effect of liposome-mediated XIAP gene transfection on hypoxia-reoxygenation-induced neonatal rat model of cardiomyocyte apoptosis by X-linked inhibitor of apoptosis protein (XIAP) Effect of Cardiomyocyte Apoptosis. Methods: The neonatal rat cardiomyocytes were cultured in vitro and divided into four groups: ① XIAP group: pDsRed2-XIAP was transfected into cardiomyocytes 48h after hypoxia for 2h-reoxygenation for 1h; ② Pretreatment group: The cells were subjected to hypoxia preconditioning and then subjected to hypoxia for 2h-reoxygenation for 1h. ③ Hypoxia-reoxygenation group: cardiomyocytes were directly subjected to hypoxia 2h-reoxygenation for 1h; normoxia group: Cans for 3h. Finally, flow cytometry Annexin V FITC was used to detect the difference of myocardial apoptosis rate in each group. Results: ①PDsRed2-XIAP could be transfected into cardiomyocytes by lipofection. ② Compared with hypoxia-reoxygenation group, the apoptosis rate of myocardial cells in XIAP group and preconditioning group was significantly decreased (P <0.01); ③ XIAP Compared with the pretreatment group, the apoptosis rate of cardiomyocytes was similar in both groups (P> 0.05). Conclusion: Physiological hypoxia 2h-reoxygenation 1h can induce apoptosis of cultured cardiomyocytes; XIAP can significantly reduce hypoxia-reoxygenation induced apoptosis of neonatal rat cardiomyocytes; XIAP apoptosis-inhibiting The effect is similar to the effect of hypoxia preconditioning in inhibiting apoptosis.