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目的探讨黄芪甲苷对阿霉素(ADR)诱导大鼠心肌细胞凋亡的抑制作用。方法采用ADR 100ng/ml(ADR1组)、250ng/ml(ADR2组)和500ng/ml(ADR3组)作用于大鼠心肌细胞株H9C2,筛查出250ng/ml为最佳实验浓度,建立ADR诱导细胞凋亡模型。用黄芪甲苷10μg/ml(黄芪甲苷1组)、25μg/ml(黄芪甲苷2组)、50μg/ml(黄芪甲苷3组)作用于ADR诱导凋亡模型细胞,筛查出50μg/ml为最佳实验浓度。培养正常H9C2细胞为对照组。测定各组细胞的凋亡率、活性氧(ROS)、线粒体膜电位(ΔΨm)水平及心肌细胞Bax、Bcl-2 mRNA的表达水平。结果与对照组比较,ADR2组细胞凋亡率升高(P<0.01);与ADR2组比较,黄芪甲苷3组细胞凋亡率降低(P<0.05)。与对照组比较,ADR2组和黄芪甲苷3组ROS水平和ΔΨm降低比例增加(P<0.05);与ADR2组比较,黄芪甲苷3组ROS水平和ΔΨm降低比例减少(P<0.05)。与对照组比较,ADR2组Bax和Bcl-2mRNA表达升高(P<0.05),Bcl-2/Bax比值下降(P<0.05);与ADR2组比较,黄芪甲苷3组Bax mRNA表达降低(P<0.01),Bcl-2 mRNA和Bcl-2/Bax比值升高(P<0.01)。结论黄芪甲苷能够抑制ADR诱导的大鼠心肌细胞的凋亡,可能是通过降低细胞内ROS水平,提高ΔΨm,降低Bax而升高Bcl-2来发挥作用。
Objective To investigate the inhibitory effect of Astragaloside IV on cardiomyocyte apoptosis induced by Adriamycin (ADR) in rats. Methods The rat cardiac muscle cell line H9C2 was treated with ADR 100ng / ml (ADR1), 250ng / ml (ADR2) and 500ng / ml (ADR3), and the optimal concentration was 250ng / Apoptosis model. Apoptosis model cells were treated with astragaloside 10μg / ml (Astragaloside 1), 25μg / ml (Astragaloside 2) and 50μg / ml (Astragaloside 3) ml for the best experimental concentration. Cultured normal H9C2 cells as control group. The apoptosis rate, reactive oxygen species (ROS), mitochondrial membrane potential (ΔΨm) and the expression of Bax and Bcl-2 mRNA in each group were measured. Results Compared with the control group, the apoptotic rate of ADR2 group was significantly increased (P <0.01). Compared with ADR2 group, the apoptosis rate of the three groups was decreased (P <0.05). Compared with control group, ROS level and ΔΨm decreased in ADR2 group and Astragaloside Ⅲ group increased (P <0.05). Compared with ADR2 group, ROS level and ΔΨm decreased proportion in Astragaloside 3 group decreased (P <0.05). Compared with the control group, the expression of Bax and Bcl-2 mRNA in ADR2 group increased (P <0.05) and the ratio of Bcl-2 / Bax decreased (P <0.05) <0.01), the ratio of Bcl-2 mRNA and Bcl-2 / Bax increased (P <0.01). Conclusion Astragaloside IV can inhibit ADR-induced apoptosis in rat cardiomyocytes, which may be through the reduction of intracellular ROS level, increase ΔΨm, decrease Bax and increase Bcl-2.