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目的观察缺血后处理对大鼠心肌缺血-再灌注损伤的保护作用,并探讨其可能的机制。方法选择Wistar大鼠24只,建立大鼠心肌缺血-再灌注损伤模型,随机分为3组:对照组(I/R组)、缺血后处理组(I-postC组)、抑制剂组(I-postC+ERK抑制剂组)。再灌注结束后腹主动脉插管取血测定血清生化指标,剖取左心室计算心肌梗死面积。结果与I/R组相比,I-postC组心肌梗死面积减少,血清乳酸脱氢酶(LDH)、心肌肌酸激酶同工酶(CK-MB)活性及丙二醛(MDA)含量降低,血清超氧化物歧化酶(SOD)活性增加;抑制剂组与I-postC组相比,心肌梗死面积增大,血清LDH、CK-MB活性及MDA含量升高,血清SOD活性减弱。结论心肌缺血后处理对实验性大鼠心肌缺血-再灌注损伤有明显的保护作用,该作用可能与细胞外调节蛋白激酶(ERK)信号传导通路有关。
Objective To observe the protective effect of ischemic postconditioning on myocardial ischemia-reperfusion injury in rats and to explore its possible mechanism. Methods Twenty-four Wistar rats were randomly divided into three groups: control group (I / R group), ischemic postconditioning group (I-postC group) and inhibitor group (I-postC + ERK inhibitor group). Serum biochemical indexes were measured after intubation of abdominal aorta by reperfusion, and left ventricular area was calculated. Results Compared with the I / R group, the area of myocardial infarction in I-postC group was decreased, the activity of serum LDH, CK-MB and the content of malondialdehyde (MDA) Serum superoxide dismutase (SOD) activity increased; inhibitor group compared with I-postC group, infarct size increased serum LDH, CK-MB activity and MDA content, serum SOD activity decreased. Conclusions Myocardial ischemic postconditioning has a protective effect on myocardial ischemia-reperfusion injury in rats, which may be related to extracellular regulated protein kinase (ERK) signal transduction pathway.