【摘 要】
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Objectives: To testify whether aerobic exercise (AE) provides cardioprotection against MI by ameliorating sympathetic nerve sprouting and myocardial beta-adrenergic receptor (AR) Signalling.Methods:Sp
【机 构】
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Institute of Sports Biology,School of Physical Education,Shaanxi Normal University,Xi'an,China
【出 处】
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International Conference for Physiological Sciences 2012(201
论文部分内容阅读
Objectives: To testify whether aerobic exercise (AE) provides cardioprotection against MI by ameliorating sympathetic nerve sprouting and myocardial beta-adrenergic receptor (AR) Signalling.Methods:Sprague-Dawley rats were randomly divided into four groups: control group (C), MI group (MC), AE with MI group (ME) and sham-operated control group (SC).Cardiac function, infarct size and pathological changes in cardiac tissue was assessed.the expression of growth associated protein 43 (GAP43), tyrosinehydroxylase(TH),Nerve growth factor(NGF), betal,beta2, beta3-AR, endothelial nitric oxide synthase(eNOS), eNOS phosphorylation(P-eNOS), neuronal nitric oxide synthase (nNOS) in the left ventricle were examined by immunocytochemical staining, immunofluoresence staining and Western blot.Results: AE improved haemodynamics, heart coefficient, decreased infarct size after MI.The GAP43, TH and NGF protein levels were suppressed, beta 1-AR was up-regulated,beta 3-AR was up-regulated, the beta2-AR was unaltered, and the expression of eNOS, P-eNOS, nNOS was up-regulated by AE after MI.Conclusion: The effects of AE on inhibiting MI-induced sympathetic nerve sprouting may be related to the inhibition of the NGF protein levels.Furthermore, the cardioprotective effects of AE are mediated by improved beta1/2-adrenoceptor balance, increased beta3-AR and rapid eNOS and nNOS activation.
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