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作 者:陈嘉勤[1] 柳维林[1] 张川湘[1] 王茂材[1] 李林[1]
出 处:《体育科学》2011年第8期53-58,共6页China Sport Science
摘 要:目的:通过中小强度有氧运动和辛伐他汀药物干预,探讨AS血管炎性损伤的修复及机制。方法:应用ApoE基因敲除和高脂高胆固醇饲料诱发小鼠AS,分为动脉硬化组、运动组、用药组;ELISA测定血清炎性因子及激素水平;免疫组化法阳性标记TLR4、NF-κb、EGF、TGF-β;RT-PCR测定CRP、MCP-1 mRNA表达。结果:12周动脉硬化组ApoE基因敲除小鼠血管可见明显斑块组织;用药组内皮表层细胞肿胀呈泡沫样,运动组则未见以上组织改变;运动和用药组小鼠血清IL-6、TNF-a含量和血管组织TLR4、NF-κb、CRP、MCP-1表达均降低(P<0.05),而血清IL-10、ET1、AngⅡ和内皮细胞EGF、TGF-βmRNA表达均升高(P<0.05)。结论:有氧运动有效防治AS小鼠血管炎性损伤,其可能机制是介导了Toll样受体通路并恢复血管激素分泌与促进内皮细胞再生。Objective: Indicated of the effects and mechanisms of atherosclerosis vascular inflammation damaged by medium-intensity aerobic exercise and simvastatin pharmaceutical on ApoE knock out mice.Methods: Induced atherosclerosis model through ApoE gene knockout and high fat and high cholesterol fed in mice,and were divided into atherosclerosis groups,exercise groups,drug groups;ELISA assay viewed of serum inflammations and hormone levels;TLR4,NF-κb,EGF,TGF-βlevels detected by immunohistochemistry assay;RT-PCR assay detection of CRP,MCP-1mRNA expression.Results: The atherosclerosis groups showed obvious plaque tissue endothelial cells on ApoE knock out mice for 12 weeks;the drug groups showed endothelial cell swelling and foamy surface,the exercise groups were no more than organizational changed.The serum of IL-6,TNF-a levels and TLR4,NF-κb,CRP,MCP-1expression in vascular of the exercise and drug groups were lower than the quite groups(P0.05),while IL-10,ET1,AngⅡ levels and EGF,TGF-β mRNA expression increased(P0.05).Conclusion: It's effectively improved vascular inflammation damaged by aerobic exercise,and the possible mechanism mediated Toll-like receptor signaling pathway,while restored hormone secretion and promoted vascular endothelial cell regeneration.
分 类 号:G804.7[文化科学—运动人体科学]
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