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目的研究参元丹后处理对大鼠心肌缺血再灌注损伤的保护作用,并尝试探讨其作用机制。方法将大鼠随机分为5组:假手术组,缺血再灌注组,缺血后处理组,参元丹0.2 g/kg组,参元丹0.1 g/kg组。采用结扎冠状动脉左前降支(LAD)建立心肌缺血再灌注模型,缺血30 min再灌注180 min,再灌注同时通过十二指肠灌注给予相应药物。常规记录Ⅱ导联心电图,分别记录再灌注期室速(VT)和室颤(VF)的发作次数、持续时间和发生率,2,3,5-氯化三苯基四氮唑(TTC)染色法法测定心肌梗死面积,化学比色法测定心肌组织超氧化物歧化酶(SOD)活力和丙二醛(MDA)含量,RT-PCR法测定组织蛋白激酶C(PKC)mRNA的表达。结果再灌注同时给予参元丹能够减少VT、VF发生次数、缩短VT、VF持续时间,有效降低心律失常发生率(P<0.05);减小心肌梗死面积;升高组织SOD活力,降低MDA含量;并增加组织中PKCαmRNA、PKCδmRNA的表达,其中参元丹0.2 g/kg组有统计学意义(P<0.05)。结论参元丹后处理具有抗心肌缺血再灌注氧化损伤的作用,其作用机制与激活PKC介导的信号转导通路有关。
Objective To study the protective effect of the senate Dan-treated on myocardial ischemia-reperfusion injury in rats and to explore its mechanism. Methods The rats were randomly divided into 5 groups: sham-operation group, ischemia-reperfusion group, ischemic postconditioning group, Shenyuandan 0.2 g / kg group and Shenyuan Dan 0.1 g / kg group. Myocardial ischemia-reperfusion model was established by ligation of the left anterior descending coronary artery (LAD), ischemia-reperfusion was performed for 30 min at 30 min, reperfusion followed by duodenal perfusion. Conventional Ⅱ lead electrocardiogram was recorded and the number of episodes, duration and incidence of ventricular tachycardia (VT) and ventricular fibrillation (VF) were recorded respectively. TTC staining The area of myocardial infarction was determined by the method of law. The activity of myocardial SOD and the content of malondialdehyde (MDA) were measured by chemical colorimetry. The expression of protein kinase C (PKC) mRNA was determined by RT-PCR. Results Shenfudan with reperfusion could reduce the number of VT and VF, shorten the duration of VT and VF, reduce the incidence of arrhythmia (P <0.05), reduce the area of myocardial infarction, increase the activity of SOD and decrease the content of MDA ; And increased the expression of PKCαmRNA and PKCδmRNA in the tissues, and the parameter of ginseng Dan 0.2 g / kg was statistically significant (P <0.05). Conclusion Senate Dan treatment has anti-myocardial ischemia reperfusion injury, its mechanism of action and activation of PKC-mediated signal transduction pathway.