低强度耐力运动加癸酸诺龙调节心脏脂联素及其受体。

A Karimi, S Joukar, H Najafipour, Y Masoumi-Ardakani, B Shahouzehi
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引用次数: 1

摘要

合成代谢雄激素类固醇(AASs)对运动员心血管系统的巨大不良影响已被报道。然而,关于所涉及的途径和机制仍然缺乏足够的信息。我们测试了脂肪联素及其在心脏中的受体可能受到长期使用AASs和锻炼的影响的假设。雄性Wistar大鼠随机分为对照(CTL)、运动(EX)、诺龙(Nan)、花生(Arach)组(以花生为载药)、训练载药(EX+Arach)组和训练诺龙(EX+Nan)组,治疗8周。实验结束一天后,动物被处死,心脏被冷冻。ELISA试剂盒定量检测心脏组织TNF-α和脂联素蛋白表达,Western blot检测脂联素受体蛋白表达。EX+Nan组TNF-α蛋白显著升高(P
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Low-intensity endurance exercise plus nandrolone decanoate modulates cardiac adiponectin and its receptors.

Vast adverse effects of anabolic-androgenic steroids (AASs) on athletes' cardiovascular systems have been reported. However, there is still a lack of adequate information regarding the pathways and mechanisms involved. We tested the hypothesis that adiponectin and its receptors in the heart may be affected by long-term use of AASs alongside exercising. Male Wistar rats were randomized into the control (CTL), exercise (EX), nandrolone (Nan), arachis (Arach) group which treated with arachis as vehicle, trained vehicle (EX+Arach) and trained nandrolone (EX+Nan) groups that were treated for 8 weeks. One day after the end of the protocol, animals were sacrificed and their hearts were frozen. TNF-α and adiponectin proteins of hearts were evaluated quantitatively by ELISA kits, and Western blot analysis was used for measuring adiponectin receptor protein expression. TNF-α protein increased significantly in the EX+Nan group (P<.05 vs CTL group). The AdipoR1 protein was significantly higher in the presence of nandrolone alongside exercise (P<.05 vs Nan and EX+Arach groups, P<.01 vs CTL and Arach groups). In addition, AdipoR2 protein enhanced in the EX+Nan group when compared with the other groups (P<.05 vs EX and EX+Arach groups, P<.01 vs CTL, Arach and Nan groups). Chronic nandrolone plus mild endurance exercise may be associated with imbalance in pro-/anti-inflammatory cytokines and may induce a positive modulatory effect on cardiac adiporeceptors in rat. Further studies are required before these findings can be generalized to humans.

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Low-intensity endurance exercise plus nandrolone decanoate modulates cardiac adiponectin and its receptors. Neuropeptide Y (NPY) inhibits spontaneous contraction of the mouse atrium by possible activation of the NPY1 receptor. Naturally occurring variants in catecholamine receptor genes. Alpha2-adrenoceptor subtypes--surprising insights from gene-targeted mouse models. NO enhances noradrenaline release: modulation and mechanism.
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