目的观察大鼠心肌短暂缺血再灌注及相应的细胞氧化应激反应对Krüppel样因子4表达的影响。方法采用短时间结扎及松解左冠状动脉前降支法构建大鼠心肌短暂缺血再灌注动物模型;采用过氧化氢(1mmol/L)处理C2C12肌原细胞法复制相应的氧化应激细胞模型;采用逆转录聚合酶链反应检测Krüppel样因子4mR-NA的表达;采用蛋白免疫印迹法检测Krüppel样因子4蛋白的表达。结果短暂缺血再灌注后,大鼠心肌组织中Krüppel样因子4mRNA的水平明显增加;过氧化氢处理C2C12肌原细胞后,Krüppel样因子4mRNA和蛋白的水平均明显增加。结论大鼠心肌短暂缺血再灌注及相应的细胞氧化应激反应均能显著诱导Krüppel样因子4的高表达。
Aim To study the effect of rat transient myocardial ischemia/reperfusion and the oxidative stress of C2C12 cells on the expression of Krüppel-like factor 4(KLF 4) gene.Methods Rat model of transient myocardial ischemia/reperfusion was established by occluding and relaxing of left coronary artery.C2C12 cells were treated with H2O2(1 mmol/L) to build the oxidative stress model.RT-PCR and Western blotting were performed to determine the changes of KLF 4 expression.Results Transient myocardial ischemia/reperfusion induced obvious accumulation of KLF 4 mRNA in rat. Oxidative stress distinctly raised the KLF 4 mRNA and protein levels in C2C12 cells. Conclusion High expression of KLF 4 gene was induced by rat transient myocardial ischemia/reperfusion and the oxidative stress of C2C12 cells.