黄芪甲苷抑制IKK/NF-κB炎症通路减轻高糖诱导的H9c2心肌细胞损伤

Astragaloside IV attenuates high glucose-induced H9c2 cardiomyocyte injury by inhibiting IKK/NF-κB inflammatory pathway

[目的]观察黄芪甲苷减轻高糖诱导H9c2细胞损伤的作用机制。[方法]通过高糖孵育诱导H9c2心肌细胞损伤模型,MTT法测定细胞存活率,酶联免疫吸附(ELISA)法检测细胞培养液上清中肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)的含量,蛋白印迹(Western Blot)法检测细胞内IκB激酶β(IKK-β)、核转录因子κB(NF-κB)、p-NF-κB及TNF-α蛋白表达水平。[结果]给予高糖处理H9c2心肌细胞12 h能明显下调细胞存活率(P<0.05);黄芪甲苷(20、40、80μmol/L)预处理10 min可呈剂量依赖性增强细胞活力,降低细胞培养液上清中TNF-α和IL-6的含量(P<0.05),下调IKK-β蛋白表达(P<0.05),抑制NF-κB磷酸活化水平(P<0.05),并降低TNF-α蛋白表达(P<0.05)。[结论]黄芪甲苷可通过抑制IKK/NF-κB炎症通路过度激活减轻高糖诱导的H9c2心肌细胞损伤。

[Objective] To observe the mechanism of astragaloside IV in alleviating H9c2 cell injury induced by high glucose.[Methods]Injured model of H9c2 cardiomyocyte was induced by high glucose. Cell viability was determined by MTT assay. TNF-α and IL-6 levels in supernatant of cell culture medium were detected by ELISA. IKK-β,NF-κB,p-NF-κB and TNF-α were detected by Western blot.[Results] High glucose treatment on H9c2 cardiomyocytes significantly down-regulated cell viability at 12 h(P<0.05);pretreatment with astragaloside(20,40,80 μmol/L) for 10 min significantly maintained cell viability,reduced the content of TNF-α and IL-6 in supernatant of cell culture medium(P<0.05),and inhibited the protein expression of IKK-β and TNF-α(P<0.05),and the activation of p-NF-κB(P<0.05).[Conclusion] Astragaloside IV alleviates high glucose-induced H9c2 cardiomyocyte injury by inhibiting the excessive activation of IKK/NF-κB inflammatory pathway.