有氧运动对ApoE基因缺陷小鼠一氧化氮系统的影响  

Effect of Aerobic Exercise on NO System in ApoE-deficient Mice

作　　者：张靓[1] 黄叔怀[2] 曾柏生[2] 

机构地区：[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

出　　处：《沈阳体育学院学报》2007年第4期4-6,共3页Journal of Shenyang Sport University

摘　　要：目的:以ApoE基因缺陷小鼠为动脉粥样硬化模型,观察有氧运动对血浆NO水平和主动脉结构型、诱导型NOS mRNA表达的变化,以探讨NO在有氧运动抑制动脉粥样硬化中的作用。方法:采用硝酸还原酶法测定血浆中NO水平,放免法测定血管壁环鸟苷酸(cyclic guanosine monophosphate,cGMP)水平,半定量RT-PCR法检测主动脉壁cNOSi、NOS的mRNA表达。结果:与对照组相比,运动组小鼠血浆NO水平升高15倍(P<0.01),血管壁cGMP活性升高90%(P<0.01),运动组小鼠主动脉壁cNOSmRNA表达显著升高,但iNOSmRNA表达无显著变化。结论:有氧运动促进了NO的合成和NOS的表达,增强血管壁对NO的反应性升高,可能是有氧运动有效防治动脉粥样硬化的机制之一。Aim：To explore the roles of NO in the inhibition effect of exercise training on atherosclerosis, we studied the changes in NO level in plasma and NOS mRNA level in the aortas in ApoE-deficient mice. Methods： ApoE deficient mice randomly were divided into control group and exercise group （swimming, 2h/d, 5d/w, 10 w）. NO level in plasma and cyclic gnanosine monophosphate （cGMP） immunoreactivity in vessel were measured. The level of cNOS and iNOS mRNA were determined by RT- PCR. Results： Compared with controls, exercise training increased NO level in plasma by 15 fold （P〈 0.01）, and the mRNA level of cNOS upregulated significantly, cGMP - ir in vessel was increased by 90 % （P〈 0.01 ）. Conclusion：exercise training increased the NO level in plasma and the cNOS tuRN level in aortas, which suggests that the improving effect of exercise training on atherosclerosis could he mediated by up regulating the NO/NOS system.

关 键 词：有氧运动 一氧化氮 结构型一氧化氮合酶 诱导型一氧化氮合酶 

分 类 号：G804.7[文化科学—运动人体科学]