丹参酮ⅡA磺酸钠注射液对亚砷酸钠导致的H9c2心肌细胞损伤的影响

Effects of sodium tanshinoneⅡA sulfonate injection on H9c2 cardiomyocyte injuryinduced by sodium arsenite

目的探究丹参酮ⅡA磺酸钠(STS)对亚砷酸钠(NaAsO2)导致的H9c2心肌细胞损伤的影响。方法采用CCK-8法检测不同浓度的STS单独处理H9c2心肌细胞后以及STS预处理后加入NaAsO2作用后的细胞活力;检测STS与NaAsO2联合作用后细胞内caspase 3/7含量;检测STS预处理后加入NaAsO2作用后细胞内caspase 8含量。结果与对照组相比,不同浓度的STS对细胞活力无明显影响(P>0.05)。与对照组相比,STS预处理组(6 h)细胞活力无明显变化(P>0.05),NaAsO2组细胞活力下降(P<0.05);与NaAsO2组相比,STS预处理组(6 h)细胞活力升高。与对照组相比,STS预处理组(12 h)和NaAsO2组细胞活力均降低(P<0.05);与NaAsO2组相比,STS预处理组(12 h)细胞活力升高(P<0.05)。STS与NaAsO2联合作用12 h后,NaAsO2组caspase 3/7含量高于NaAsO2+STS组、对照组和STS组,差异均有统计学意义(P<0.05)。STS预处理12 h后加入NaAsO2作用24 h,NaAsO2组caspase 8含量与其他组相比无统计学差异(P>0.05)。结论STS可以减轻NaAsO2对H9c2心肌细胞的损伤。

Objective To investigate the effects of sodium tanshinoneⅡA sulfonate(STS)on H9c2 cardiomyocyte injury induced by sodium arsenite(NaAsO2).Methods CCK-8 assay was used to detect viability of H9c2 cardiomyocytes treated with different concentrations of STS.Cell viability was also assessed in H9c2 cardiomyocytes treated with NaAsO2 after STS pretreatment using a CCK-8 kit.Apoptosis of H9c2 cardiomyocytes treated with STS and NaAsO2 was measured.Caspase 8 abundance was quantitated in H9c2 cardiomyocytes.Results Compared with a vehicle control group,there was no significant change in cell viability among H9c2 cardiomyocytes treated with different concentrations of STS alone.Compared with cells untreated with NaAsO2,there was no significant difference in the viability of cells pretreated with STS(6 h),whereas cell viability was significantly decreased in the NaAsO2 group.Viability was decreased in cells pretreated with STS(12 h)followed by exposure to NaAsO2.Viability in the STS pretreatment groups(6 h and 12 h)was significantly increased compared to viability in the NaAsO2 group.Caspase 3/7 content in the NaAsO2 group was higher than that in the NaAsO2+STS group,the vehicle control group,and the STS group.No significant difference was observed in caspase 8 abundance between the NaAsO2 group and other groups.Conclusion STS can attenuate NaAsO2-induced injury in H9c2 cardiomyocytes.