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IL-6预处理保护H_2O_2致心肌细胞损伤作用机制初探 被引量:4

The mechanism of pretreatment with IL-6 on the myocardial cells injury induced by H_2O_2
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摘要 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 study the effect of pretreatment with IL-6 on H2O2 induced myocardial oxidative stress injury in rats.Methods H2O2 was used to stimulate the primary cultured myocardial cells to establish cellular oxidative stress model.The cell viability was checked by MTT assay.AnnexinV-FITC staining and flow cytometry were used to detect cell apoptosis.The expression of myocardial intracellular GSH,SOD and MDA was detected.Results H2O2 can reduce the cell viability and increase the rate of apoptosis.IL-6 pretreatment significantly improved cell viability and reduce apoptosis(P〈0.05).Low concentrations of IL-6 significantly increased the intracellular levels of GSH and SOD,but decreased the level of MDA,while with increasing the concentration of IL-6,this effect was gradually disappeared.Conclusion Pretreatment with IL-6 can protect the myocardial cells injury induced by H2O2,which may be associated with the change in the expression levels of GSH,SOD and MDA.
出处 《热带医学杂志》 CAS 2011年第9期1014-1017,共4页 Journal of Tropical Medicine
基金 国家自然科学基金(30572435)
关键词 氧化应激 IL-6 心肌细胞 凋亡 oxidative stress IL-6 myocardial cells apoptosis
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