摘要
目的:探讨蛋白激酶C(PKC)与大鼠心肌缝隙连接蛋白43(Cx43)在晚期运动预处理(LEP)心肌保护效应中的关系及相互影响。方法:48只SD大鼠分为对照组(C组)、力竭运动组(EE组)、晚期运动预处理组(LEP组)、白屈菜赤碱+晚期运动预处理组(CHE+LEP组)、晚期运动预处理+力竭运动组(LEP+EE组)和白屈菜赤碱+晚期运动预处理+力竭运动组(CHE+LEP+EE组),每组8只。在进行LEP或/和PKC特异性抑制剂CHE干预后运动至力竭,观察、检测心肌Cx43 m RNA和蛋白的分布情况及表达变化。结果:⑴各组Cx43 m RNA原位杂交信号未见明显差异,实时荧光定量PCR结果亦无显著差异。⑵CHE+LEP组Cx43免疫阳性表达较LEP组减弱,CHE+LEP+EE组Cx43免疫阳性表达较LEP+EE组减弱;CHE+LEP组Cx43蛋白表达较LEP组显著降低,CHE+LEP+EE组Cx43蛋白表达较LEP+EE组显著降低。结论:在晚期运动预处理心肌保护效应信号转导通路中,PKC是心肌Cx43的上游中介物质。
Objective This study intends to probe into the effect of protein kinase C(PKC)on the expression of myocardial connexin 43(Cx43)during late exercise preconditioning(EP). Methods 48 SD rats were randomly divided into control group(C),exhaustive exercise group(EE),late exercise preconditioning group(LEP),chelerythrine(CHE)treating and late exercise preconditioning group(CHE+LEP),late exercise preconditioning and exhaustive exercise group(LEP+EE),and CHE treating and late exercise preconditioning plus exhaustive exercise group(CHE+LEP+EE). The expression of myocardial Cx43 m RNA and protein in the rats was detected.The model of LEP was established by 4-repeated interval treadmill running at the speed of 28-30m/min for 10 min with an interval of 10 min. Results(1)There was no significant difference in in situ hybridization signal in all groups,and in the expression of myocardial Cx43 m RNA in groups CHE+LEP and CHE+LEP+EE.(2)The immune positive expression of Cx43 was lower in group CHE+LEP than in group LEP,and in group CHE+LEP+EE was lower than in group LEP+EE. Conclusion Protein kinase C seems to be the upstream mediator of myocardial Cx43 in the signal transduction pathway under the protective effect of late exercise preconditioning.
出处
《中国运动医学杂志》
CAS
北大核心
2015年第11期1079-1084,1097,共7页
Chinese Journal of Sports Medicine
基金
中国博士后科学基金
曲阜师范大学博士科研启动基金