缓激肽对氧化应激反应诱导的心肌细胞衰老影响的临床研究

Clinical Study on the Effect of Bradykinin on Oxidative Stress-induced Myocardial Cell Aging

目的分析缓激肽对氧化应激反应诱导的心肌细胞衰老的影响。方法通过细胞培养的方法进行研究,将氧化应激反应诱导的衰老的心肌细胞按照处理方法不同分为3组:正常细胞组、缓激肽组和对照组,各35个心肌细胞数。其中正常细胞组未加入过氧化氢对细胞进行诱导,单纯加入缓激肽;缓激肽组将缓激肽加入由过氧化氢氧化诱导的衰老的H9C2细胞;对照组单纯接受过氧化氢诱导的H9C2细胞,未加入缓激肽。结果随着缓激肽的浓度增加,衰老细胞的个数呈现下降的趋势,不同浓度缓激肽之间衰老细胞对比差异有统计学意义(P<0.01)。正常细胞组细胞衰老率显著低于缓激肽组和对照组(P<0.01),缓激肽组细胞衰老率显著低于对照组(P<0.01)。3组Oliver尾含量比较差异有统计学意义(P<0.01),缓激肽组Oliver尾含量显著低于对照组(P<0.01),但高于正常细胞组(P<0.01)。结论缓激肽能够有效保护由氧化应激反应诱导的心肌细胞的衰老,能够抑制氧化应激反应对心肌细胞DNA的损伤程度。

Objective To analyze the effect of bradykinin on oxidative stress-induced myocardial cell aging. Methods Cultured samples of oxidative stress-induced aging myocardial cells were divided into normal cells group,bradykinin group and control group,with 35 myocardial cells in each group. Cells in normal cells group were not induced by hydrogen peroxide but singly by bradykinin; bradykinin was added to the aging H9C2 cells in bradykinin group induced by hydrogen peroxide; and H9C2 cells in control group were singly induced by hydrogen peroxide,without adding bradykinin. Results With increasing concentrations of bradykinin,the number of aging cells showed a downward trend,differences of the aging cell numbers between different concentrations of bradykinin were statistically significant（ P〈0. 01）. The aging rate of cells in normal cells group was significantly lower than those of bradykinin group and control group（ P〈0. 01）;aging rate of cells in bradykinin group was significantly lower than the control group（ P〈0. 01）. Differences of Oliver ending contents between either two of three groups were statistically significant（ P〈0. 01）,Oliver ending content of bradykinin group was significantly lower than the control group（ P〈0. 01）,while higher than normal cells group（ P〈0. 01）. Conclusion Bradykinin can effectively protect the oxidative stress-induced myocardial cell from aging,and inhibit the DNA damage to myocardial cells caused by oxidative stress.