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有氧运动抗ApoE-/-小鼠动脉粥样硬化的L-精氨酸机制探讨
引用本文:张靓,黄叔怀,曾柏生.有氧运动抗ApoE-/-小鼠动脉粥样硬化的L-精氨酸机制探讨[J].北京体育大学学报,2008,31(3):336-338.
作者姓名:张靓  黄叔怀  曾柏生
作者单位:1. 北京师范大学体育与运动学院,北京,100875
2. 扬州大学体育学院,江苏,扬州,225002
基金项目:国家自然科学基金青年科学基金项目(30600232)资助
摘    要:目的:以ApoE基因缺陷小鼠为动脉粥样硬化模型,观察有氧运动对小鼠动脉粥样硬化斑块的作用,及运动对血浆一氧化氮(nitric oxide,NO)、血浆L-精氨酸(L-arginine,L-Arg)与不对称二甲基精氨酸(asymmetricdimethlarginine,ADMA)比值的影响,以探讨NO及其底物L-Arg在运动抗动脉粥样硬化中的作用。方法:ApoE基因缺陷小鼠随机分为安静对照组和运动组(游泳运动,2 h/次,5次/周,共10周),分别测定粥样斑块面积,采用硝酸还原酶法测定血浆中NO水平,利用高效液相法测定血清中ADMA与L-Arg的水平,另对血清肌酐和肾脏超微结构进行观察。结果:与对照组相比,运动组小鼠斑块面积显著减小40%(P<0.01),小鼠血浆NO水平升高15倍(P<0.01),L-Arg/ADMA比值显著升高10%(P<0.05)。结论:有氧运动使血浆L-Arg/ADMA比值升高,促进L-Arg的利用,NO合成增多,可能是运动抗动脉粥样硬化的机制之一。

关 键 词:有氧运动  动脉粥样硬化  ADMA  L-Arg
文章编号:1007-3612(2008)03-0336-03
修稿时间:2007年5月28日

Effect of Mechanism of L-Arg of Aerobic Exercise on Anti-ApoE-Deficient Mice Antherosclerosis
ZHANG Jing,HUANG Shu-huai,ZENG Bai-sheng.Effect of Mechanism of L-Arg of Aerobic Exercise on Anti-ApoE-Deficient Mice Antherosclerosis[J].Journal of Beijing Sport University,2008,31(3):336-338.
Authors:ZHANG Jing  HUANG Shu-huai  ZENG Bai-sheng
Abstract:To explore the roles of nitric oxide(NO) and L-arginine(L-Arg) in the anti-atherosclerosis effects of aerobic exercise,we study the changes in atherosclerotic plaue area in aortic sinuses and the plasma NO,L-Arg and asymmetric dimethlarginine(ADMA) ratio in ApoE deficient mice.Methods: ApoE deficient mice are randomly divided into control group and exercise group(swimming,2h/d,5d/w,10 w).Atherosclerotic plaue area in aortic sinuses and NO level in plasma are measured.Plasma L-Arg and ADMA are determined by HPLC method,and ultrastructures of kidney are observed by transmission electron microscope.Results: Compared with controls,exercise training decreases the lesion area by 40%(P<0.01), and NO level in plasma increases by 15 folds(P<0.01).L-Arg/ADMA in plasma is increased by 10%(P<0.05).Conclusion: aerobic exercise decreases ADMA level,improves the utilization of L-Arg and increases the synthesis of NO,which suggests that the anti-antherosclerosis effect on aerobic exercise may be mediated by upregulating the utilization of L-Arg.
Keywords:aerobic exercise  antherosclerosis  ADMA  L-Arg
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