磷酸肌酸钠对力竭运动大鼠心肌线粒体解偶联蛋白2和能量代谢变化的影响

发布时间：2018-03-21 15:10

本文选题：解偶联蛋白　切入点：猝死　出处：《解放军医学杂志》2015年11期 　论文类型：期刊论文

【摘要】：目的探讨磷酸肌酸钠对一次力竭运动大鼠心肌线粒体能量代谢变化的影响,探讨磷酸肌酸钠对应激心肌的保护机制。方法雄性Wistar大鼠36只,随机分为对照组(n=12)、一次力竭组(n=12)、磷酸肌酸钠组(n=12)。实验结束后测定各组心肌ATP含量及血浆肾上腺素(E)、去甲肾上腺素(NE)、游离脂肪酸(FFA)浓度,并采用RT-PCR及Western blotting检测心肌线粒体解偶联蛋白2(UCP2)表达情况。结果与对照组相比,一次力竭组、磷酸肌酸钠组血浆FFA、E、NE浓度均增高(P0.05),心肌ATP含量均降低。RT-PCR及Western blotting结果显示,一次力竭组、磷酸肌酸钠组UCP2 m RNA表达量分别较对照组增加64%、24%,UCP2蛋白表达量分别较对照组增加65%、26%。相关分析显示,心肌组织UCP2表达量与血浆FFA浓度呈显著正相关(r=0.98,P0.01),血浆FFA浓度与血浆E、NE水平呈显著正相关(r=0.93,r=0.88,P0.01)。结论力竭运动后心肌组织UCP2表达量显著上调,ATP合成减少,能量代谢障碍,可能是运动导致心源性猝死的机制之一。补充外源性磷酸肌酸钠可拮抗运动应激导致的UCP2表达升高,增加ATP储备,改善心肌能量代谢,可能对运动导致的心源性猝死预防有一定的积极作用。
[Abstract]:Objective to investigate the effect of sodium phosphocreatine exhaustion of energy metabolism of myocardial mitochondria in rats on a moving force, and investigate the protective effects of creatine phosphate sodium stress myocardium. Methods 36 male Wistar rats were randomly divided into control group (n=12), exhaustive group (n=12), creatine phosphate sodium group (n=12) determination of myocardial ATP content and plasma epinephrine group after the experiment (E), norepinephrine (NE), free fatty acid (FFA) concentration, and using RT-PCR and Western blotting to detect myocardial mitochondrial uncoupling protein 2 (UCP2) expression. Results compared with the control group, exhaustive group, creatine phosphate sodium group plasma FFA, E, NE concentrations were significantly increased (P0.05), myocardial ATP content decreased.RT-PCR and Western blotting results showed that the exhaustive group, the expression of UCP2 m RNA creatine phosphate group were higher than that of control group 64%, 24%, UCP2 protein expression were compared with the control group increased 6 5%, the 26%. correlation analysis showed that the myocardial tissue was positively related to the expression of UCP2 and plasma concentration of FFA (r=0.98, P0.01), the concentration of plasma FFA and plasma E, NE levels were positively correlated (r=0.93, r=0.88, P0.01). Conclusion the exhaustion of myocardial UCP2 expression was significantly increased after exercise, reducing the synthesis of ATP energy, metabolic disorders, may be one of the mechanisms leading to sudden cardiac death. The supplement of exogenous creatine phosphate sodium can lead to antagonistic exercise stress increased the expression of UCP2, ATP increase in reserves, improve myocardial energy metabolism, cardiac sudden death caused by the movement of a certain positive role in prevention.

【作者单位】：济南军区总医院心内科;辽宁医学院研究生院;
【基金】：2014全军后勤科研重大项目子项目(AWS13C008)~~
【分类号】：R87

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