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目的初步探讨IL-6预处理对H2O2致心肌细胞氧化应激损伤的作用机制。方法采用心肌细胞原代培养方法,以H2O2刺激心肌细胞,建立细胞氧化应激模型;采用MTT法检测细胞活力;AnnexinV-FITC染色法和流式细胞术检测细胞凋亡率;检测心肌细胞内谷胱甘肽(GSH)、超氧化物歧化酶(SOD)、丙二醛(MDA)的表达情况。结果 H2O2可降低心肌细胞存活率并能增加其凋亡,IL-6预处理后能显著改善细胞活力及凋亡情况,与模型组相比差异有统计学意义(P<0.05)。低浓度IL-6能明显增加细胞内GSH与SOD的水平,并降低MDA的含量,随着IL-6浓度的增加,这种效应逐渐消失。结论 IL-6预处理能保护H2O2致心肌细胞损伤作用,这可能与IL-6调节细胞GSH、SOD、MDA表达有关。
Objective To investigate the mechanism of IL-6 preconditioning on H2O2-induced oxidative stress injury in cardiomyocytes. Methods Primary cultured cardiomyocytes were used to stimulate cardiomyocytes with H2O2 to establish oxidative stress model. Cell viability was measured by MTT assay. Apoptosis rate was detected by Annexin V-FITC staining and flow cytometry. (GSH), superoxide dismutase (SOD) and malondialdehyde (MDA) in the rats. Results H2O2 could reduce the survival rate of cardiomyocytes and increase its apoptosis. After pretreatment with IL-6, the viability and apoptosis of cells were significantly improved, which was significantly different from that of model group (P <0.05). Low concentrations of IL-6 could significantly increase the level of intracellular GSH and SOD, and reduce the content of MDA, with the IL-6 concentration increased, this effect gradually disappeared. Conclusion IL-6 preconditioning can protect H2O2 -induced cardiomyocyte injury, which may be related to the expression of GSH, SOD and MDA in IL-6-regulated cells.