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目的:探讨血红素氧合酶-1(HO-1)在运动预适应(EP)中对大鼠心肌相对缺血再灌注(rI/R)损伤的延迟保护作用及机制。方法:40只W istar大鼠随机分为5组:正常对照组(CN)、相对缺血再灌注组(IR)、运动预适应+相对缺血再灌注组(EI)、Hem in(HO-1诱导剂)+相对缺血再灌注组(HE)和运动预适应+ZnPP(HO-1抑制剂)+相对缺血再灌注组(EZ)。测定大鼠再灌注期心率脉压乘积(PRP)、冠脉流出液MDA含量、HO-1活性等。结果:心肌HO-1活性:EI组和HE组较IR组显著升高,EZ组则显著降低。EZ组较EI组显著降低,EI组和HE组间亦有显著差异。再灌注后60 m in时点PRP恢复率:EI组较IR组显著增高;IR组与HE组未见显著差异,但30 m in时点HE组显著增高;EZ组较EI组显著降低。冠脉流出液MDA含量:EI组、EZ组和HE组MDA含量较IR组皆显著降低;EZ组较EI组显著升高。结论:EP可以诱导HO-1合成,进而通过HO-1对24 h后发生的rI/R损伤产生延迟保护作用。
Objective: To investigate the delayed protective effect of heme oxygenase-1 (HO-1) on myocardial ischemia-reperfusion (rI / R) injury induced by exercise preconditioning (EP) and its mechanism. Methods: Forty Wistar rats were randomly divided into 5 groups: normal control group (CN), relative ischemia-reperfusion group (IR), preconditioning + relative ischemia-reperfusion group (EI), Hem in 1 inducer) + relative ischemia reperfusion group (HE) and exercise preconditioning + ZnPP (inhibitor of HO-1) + relative ischemia reperfusion group (EZ). The rat heart rate pulse pressure product (PRP), coronary effluent MDA content and HO-1 activity were measured. Results: HO-1 activity in myocardium was significantly higher in EI group and HE group than in IR group and significantly lower in EZ group. EZ group was significantly lower than EI group, EI group and HE group also have significant differences. The recovery rate of PRP at 60 mins after reperfusion was significantly higher in EI group than that in IR group, but no significant difference was found between IR group and HE group, but the HE group was significantly increased at 30 m in. EZ group was significantly lower than EI group. MDA content in coronary effluent: MDA content in EI group, EZ group and HE group were significantly lower than those in IR group; EZ group was significantly higher than EI group. CONCLUSION: EP can induce HO-1 synthesis and then delay the protective effect of HO-1 against rI / R injury after 24 h.