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去氢表雄酮和抗阻训练引起心脏重构:胎儿基因的作用及其对心脏病理生理学的影响。

Nandrolone and resistance training induce heart remodeling: role of fetal genes and implications for cardiac pathophysiology.

机构信息

Department of Physiological Sciences, Piracicaba Dental School, University of Campinas, Piracicaba, SP, Brazil.

出版信息

Life Sci. 2011 Oct 24;89(17-18):631-7. doi: 10.1016/j.lfs.2011.08.004. Epub 2011 Aug 17.

DOI:10.1016/j.lfs.2011.08.004
PMID:21889516
Abstract

AIMS

This study was conducted to assess the isolated and combined effects of nandrolone and resistance training on cardiac morphology, function, and mRNA expression of pathological cardiac hypertrophy markers.

MAIN METHODS

Wistar rats were randomly divided into four groups and submitted to 6 weeks of treatment with nandrolone and/or resistance training. Cardiac parameters were determined by echocardiography. Heart was analyzed for collagen infiltration. Real-time RT-PCR was used to assess the pathological cardiac hypertrophy markers.

KEY FINDINGS

Both resistance training and nandrolone induced cardiac hypertrophy. Nandrolone increased the cardiac collagen content, and reduced the cardiac index in non-trained and trained groups, when compared with the respective vehicle-treated groups. Nandrolone reduced the ratio of maximum early to late transmitral flow velocity in non-trained and trained groups, when compared with the respective vehicle-treated groups. Nandrolone reduced the alpha-myosin heavy chain gene expression in both non-trained and trained groups, when compared with the respective vehicle-treated groups. Training reduced the beta-myosin heavy chain gene expression in the groups treated with vehicle and nandrolone. Only the association between training and nandrolone increased the expression of the skeletal alpha-actin gene and atrial natriuretic peptide in the left ventricle.

SIGNIFICANCE

This study indicated that nandrolone, whether associated with resistance training or not, induces cardiac hypertrophy, which is associated with enhanced collagen content, re-expression of fetal genes the in left ventricle, and impaired diastolic and systolic function.

摘要

目的

本研究旨在评估去甲雄酮和抗阻训练对心脏形态、功能以及病理性心肌肥厚标志物的 mRNA 表达的单独和联合作用。

主要方法

Wistar 大鼠随机分为 4 组,接受 6 周的去甲雄酮和/或抗阻训练治疗。采用超声心动图检测心脏参数。分析心脏胶原浸润情况。实时 RT-PCR 检测病理性心肌肥厚标志物。

主要发现

抗阻训练和去甲雄酮均可诱导心脏肥大。与相应的载体处理组相比,去甲雄酮增加了非训练和训练组的心脏胶原含量,并降低了心脏指数。与相应的载体处理组相比,去甲雄酮降低了非训练和训练组的最大早期至晚期二尖瓣血流速度比值。与相应的载体处理组相比,去甲雄酮降低了非训练和训练组的α-肌球蛋白重链基因表达。与载体处理组相比,训练降低了β-肌球蛋白重链基因在各组中的表达。只有训练和去甲雄酮的联合增加了左心室骨骼肌α-肌动蛋白基因和心钠肽的表达。

意义

本研究表明,去甲雄酮,无论是否与抗阻训练联合应用,均可诱导心脏肥大,其特征是胶原含量增加,左心室中胎儿基因的重新表达,以及舒张和收缩功能受损。

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