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目的观察缺血后处置对大鼠心肌缺血/再灌注损伤的影响,并初步探讨其作用机制。方法复制离体大鼠心肌缺血/再灌注损伤模型及缺血后处置模型。记录±dp/dtmax和LVEDP。用比色法检测灌流液中乳酸脱氢酶(LDH)、丙二醛(MDA)水平及超氧化物歧化酶(SOD)活性,Western blot方法检测心脏eNOS及ERK1/2的表达,RT-PCR方法测定心脏细胞色素P4502J3(CYP2J3)mRNA表达。结果与缺血/再灌注组(IR)相比,缺血后处置组(IPo)±dp/dtmax均增高(P<0.01),而LVEDP、LDH降低(P<0.05);IR组MDA水平高于对照组(CON)及IPo组(P<0.01),SOD活性低于IPo组(P<0.01);IR组大鼠心肌eNOS及磷酸化ERK1/2的表达均高于CON组和IPo组;IPo组大鼠心脏CYP2J3 mRNA的表达明显高于CON组和IR组。结论缺血后处置可能通过提高再灌注心肌SOD活性,增加氧自由基清除,而改善缺血/再灌注引起的心功能障碍及细胞损伤;CYP2J3/EET系统有可能参与其保护作用。
Objective To observe the effect of ischemic postconditioning on myocardial ischemia / reperfusion injury in rats and to explore its mechanism. Methods Myocardial ischemia-reperfusion injury model and ischemic postconditioning model in vitro were duplicated. Record ± dp / dtmax and LVEDP. The levels of LDH, MDA and SOD in the perfusate were detected by colorimetric method. The expressions of eNOS and ERK1 / 2 in heart were detected by Western blot. Methods The cardiac cytochrome P4502J3 (CYP2J3) mRNA expression was measured. Results Compared with the ischemia / reperfusion group, the ± dp / dtmax of IPo increased (P <0.01) and the LVEDP and LDH decreased (P <0.05) The levels of eNOS and phosphorylated ERK1 / 2 in myocardium of IR group were higher than that of CON group and IPo group in CON group and IPo group (P <0.01) The expression of CYP2J3 mRNA in IPo group was significantly higher than that in CON group and IR group. Conclusions Post-ischemic postconditioning may improve cardiac function and cell injury induced by ischemia / reperfusion by increasing the activity of SOD in myocardial reperfused myocardium and increasing the clearance of oxygen free radicals. CYP2J3 / EET may play a protective role.