目的:探讨运动预适应(EP)对力竭所致心肌损伤的晚期保护效应中心肌εPKC表达变化。方法:SD大鼠分为对照组(C组)、力竭运动组(EE组)、晚期运动预适应组(LEP组)、晚期运动预适应+力竭运动组(LEP+EE组)。在EP模型基础上,用力竭跑台运动致大鼠心肌损伤。用免疫化学发光法检测血清cTnI的含量;用免疫印迹法与免疫组织化学法检测心肌εPKC定量与定位表达变化。结果:与C组比,EE组血清cTnI水平、εPKC蛋白水平显著升高,免疫反应阳性于心肌闰盘聚集;LEP组血清cTnI无明显变化,εPKC蛋白水平显著升高,免疫反应阳性于心肌闰盘聚集。与EE组比,LEP+EE组血清cTnI水平显著下降,蛋白水平无明显变化,免疫反应阳性未在心肌闰盘聚集。结论:εPKC参与了EP对力竭运动致心肌损伤的晚期保护效应。
Objective : To determine whether exercise preconditioning (EP) is capable of protecting myocardium from exhaustive exercise and view the change of cPKC expression during exercise preconditioning. Methods:SD rats were divided into control group(C),EE group, LEP group, LEP+EE group. After establishing of EP animal model, exhaustive exercise on treadmill for inducing myocardial injury. Then the level of cTnI was detected by chemiluminescent immunoassay. Western blotting method was used to detect changes of cPKC, immunohistochemistry method was used to observe expressions of cPKC. Results:As compared with the group C, the cTnI level in serum increased significantly, εPKC significantly increased and εPKC translocated from the soluble to the intercalated disk in group EE. While compared with the group C, there was no significant difference in the cTnI level in group LEP, but εPKC significantly increased and the cPKC translocated from the soluble to the intercalated disk. As com- pared with the group EE, the cTnI level in serum decreased significantly in group LEP+ EE, there was no significant difference in cPKC level and there was no expression at intercalated disk. Conclusion:Exercise preconditioning induced-late myocardial protection against exhaustive exercise injury and cPKC participated in late cardioprotection induced by exercise precondition- ing.