目的 探讨心肌缺血再灌注过程中蛋白激酶C(PKC)活性变化对缺血再灌注损伤心肌的影响及机制.方法 将40只大鼠随机分为模型组、观察1组、观察2组及对照组各10只,前三组均采用冠状动脉分支结扎术制备心肌缺血再灌注模型,再灌注1 h后结束实验;其中观察1组和观察2组分别于冠状动脉结扎术前20 min经股静脉注射佛波酯及多黏菌素B;对照组为假手术组.实验结束后各组均取静脉血,采用化学比色法测定肌酸激酶(CK)和丙二醛(MDA)水平;处死动物,取心肌组织,采用免疫组化法检测PKC和环氧化酶-2(COX-2)表达.结果 与对照组比较,模型组血清CK、MDA水平明显升高(P＜0.01),心肌PKC表达无明显差异、COX-2表达明显升高(P＜0.05);与观察2组相比,观察1组血清CK、MDA水平明显降低(P＜0.05),心肌PKC 表达明显升高、COX-2表达明显降低(P均＜0.01).结论 PKC激活有利于减轻心肌氧化应激损伤,可能机制为下调COX-2表达;此为心肌缺血再灌注损伤的防治提供了依据.%Objective To investigate the effect and mechanism of protein kinase C (PKC) on myocardial ischemia reperfusion. Methods Forty rats were randomly divided into model group, observation group 1, observation group 2 and control group with 10 in each. Model of myocardial ischemia by coronary artery ligation was prepared in the first three groups, and then followed by repeffusing for 1 hour. Observation group 1 and 2 were injected with phorbol ester and polymyxin B through femoral vein about 20 min before coronary artery ligation. The control group was sham-operated group. Venous blood was collected after the experiment, the concentration of creatine kinase (CK) and malondialdehyde (MDA)were detected by chemical colorimetry; myocardium was obtained after the rats were executed, then the expression of PKC and cyclooxygenase-2 (COX-2) were detected by immunohistochemistry. Results Compared with the control group, concentration of serum CK, MDA in model group were significantly higher ( P ＜ 0.01 ), PKC expression was not significantly different, but the COX-2 expression was significantly higher ( P ＜ 0.01 ); compared with observation group 2, concentration of serum CK, MDA concentration in observation group 1 decreased significantly (P ＜ 0.05 ), PKC expression was significantly higher, COX-2 expression was significantly lower ( both P ＜ 0.01 ). Conclusions PKC activation is conducive to reduce myocardial oxidative stress, the possible mechanism is to decrease the expression of COX-2; this study can provide basis for the myocardial ischemia reperfusion.
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