EGCG对高糖诱导的大鼠H9C2心肌细胞损伤的改善作用研究

Study on the ameliorative effect of EGCG on high glucose-induced injury in rat H9C2 cardiomyocytes

研究了表没食子儿茶素没食子酸酯(Epigallocatechin gallate,EGCG)对高糖诱导受损的大鼠心肌细胞(H9C2)的改善作用及其分子机制.采用高糖培养液建立高糖细胞损伤模型,检测了EGCG给药处理后对细胞活力、抗氧化酶活性SOD和GSH-Px、促炎因子TNF-α和IL-6水平、相关mRNA转录水平(NF-κB、IκBα和IL-1β).结果表明:与正常组相比,模型组心肌细胞活力显著下降、SOD和GSH-Px活性均显著降低,TNF-α和IL-6炎性因子水平显著增加,NF-κB、IκBα和IL-1βmRNA转录水平显著上调(P<0.01);与高糖组相比,EGCG预处理后可显著增加细胞活力水平,显著增加细胞SOD和GSH-Px活性,显著降低TNF-α和IL-6炎性因子水平,显著下调NF-κB、IκBα和IL-1βmRNA转录水平降(P<0.01).EGCG能够减轻高糖诱导的H9C2心肌细胞损伤,降低细胞炎症反应,其机制可能与NF-κB炎症信号通路有关.

To investigate the ameliorative effect of epigallocatechin gallate(EGCG)on high glucose-induced damaged rat cardiomyocytes(H9C2)and its molecular mechanism.A high-glucose cell injury model was established using high-glucose culture medium,and the effects of EGCG administration treatment on cell viability,antioxidant enzyme activities SOD and GSH-Px,pro-inflammatory factors TNF-αand IL-6 levels,and related mRNA transcript levels(NF-κB,IκBαand IL-1β)were examined.The results showed that cardiomyocyte viability,SOD and GSH-Px activities were significantly decreased,TNF-αand IL-6 inflammatory factor levels were significantly increased,and NF-κB,IκBαand IL-1βmRNA transcript levels were significantly upregulated in the model group compared with the normal group(P<0.01).EGCG pretreatment significantly increased cell viability levels,significantly increased cellular SOD and GSH-Px activities,significantly decreased TNF-αand IL-6 inflammatory factor levels,and significantly downregulated NF-κB,IκBα,and IL-1βmRNA transcript levels down compared to the high glucose group(P<0.01).EGCG was able to attenuate high glucose-induced H9C2 cardiomyocyte injury and reduce the cellular inflammatory response by a mechanism that may be related to the NF-κB inflammatory signaling pathway.