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目的研究短期运动对大鼠心肌缺血再灌注损伤的保护作用及与蛋白激酶C(PKC)和锰超氧化物歧化酶(MnSOD)的关系。方法72只Wistar大鼠随机分为4组:对照组(CON组)、运动组(EXE组)、运动+PKC抑制剂CHE组(E+C组)和PKC抑制剂组(CHE组)。以上4组大鼠每组再随机分成2组:(1)I/R组:应用Langendorff离体心脏缺血/再灌注模型,观察各组大鼠再灌注期间心功能指标恢复率及心肌梗死范围;(2)假处理组:取左心室心肌组织进行MnSOD活性测定。结果EXE组大鼠左心室发展压(LVDP)和心率压力乘积(RPP)的恢复率明显高于CON组和E+C组(P<0.05或<0.01),心肌梗死范围显著低于CON组和E+C组(均P<0.01);CON组和CHE组上述指标无明显差异(P>0.05)。EXE组大鼠心肌组织MnSOD活性高于CON组和E+C组(P<0.05),CHE组和CON组MnSOD活性无明显差异(P>0.05)。结论短期运动通过激活PKC、升高MnSOD活性,发挥对心肌缺血/再灌注损伤的保护作用;PKC是MnSOD活性升高的中间信号分子。
Objective To investigate the protective effect of short-term exercise on myocardial ischemia-reperfusion injury and its relationship with protein kinase C (PKC) and manganese superoxide dismutase (MnSOD). Methods 72 Wistar rats were randomly divided into 4 groups: control group (CON group), exercise group (EXE group), exercise + PKC inhibitor CHE group (E + C group) and PKC inhibitor group (CHE group). The above four groups of rats were randomly divided into two groups: (1) I / R group: Langendorff isolated heart ischemia / reperfusion model was used to observe the recovery rate of cardiac function and myocardial infarction ; (2) sham-treated group: MnSOD activity was measured in left ventricular myocardium. Results The recovery rate of LVDP and RPP in EXE group was significantly higher than that in CON group and E + C group (P <0.05 or <0.01). The extent of myocardial infarction was significantly lower than that in CON group and E + C (all P <0.01). There was no significant difference between CON and CHE (P> 0.05). MnSOD activity in myocardium of EXE group was higher than that of CON group and E + C group (P <0.05). MnSOD activity of CHE group and CON group had no significant difference (P> 0.05). Conclusion Short-term exercise can activate PKC and increase MnSOD activity, which can protect myocardial ischemia / reperfusion injury. PKC is an intermediate signaling molecule with increased MnSOD activity.