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目的观察吡格列酮对大鼠心肌细胞缺血再灌注(I/R)损伤(MIRI)后GRP78和caspase-12蛋白表达的影响,探讨吡格列酮内质网应激途径的心肌保护。方法 Wistar大鼠30只随机分为I/R+Pio组[灌服5mg/(kg.d)]、I/R组及假手术组,各10只。制作大鼠心肌再灌注损伤模型。TUNEL检测心肌细胞凋亡,免疫组织化学检测GRP78和caspase-12表达变化。结果吡格列酮预处理组大鼠心肌细胞凋亡及GRP78、caspase-12蛋白表达水平明显比I/R组减少(P<0.05)。结论通过内质网应激途径可能是吡格列酮对心肌再灌注损伤的保护作用机制之一。
Objective To observe the effect of pioglitazone on the expression of GRP78 and caspase-12 protein after myocardial ischemia-reperfusion (I / R) injury in rats (MIRI) and explore the protective effect of pioglitazone on endoplasmic reticulum stress. Methods Thirty Wistar rats were randomly divided into I / R + Pio group (5 mg / (kg.d), I / R group and sham operation group, 10 rats in each group). Rat model of myocardial reperfusion injury was made. Cardiomyocyte apoptosis was detected by TUNEL and the expression of GRP78 and caspase-12 was detected by immunohistochemistry. Results The apoptosis and the expression of GRP78 and caspase-12 in pioglitazone preconditioning group were significantly lower than those in I / R group (P <0.05). Conclusion The mechanism of the protective effect of pioglitazone on myocardial reperfusion injury may be through the endoplasmic reticulum stress pathway.