Nandrolone attenuates aortic adaptation to exercise in rats

Nandrolone
DOI: 10.1093/cvr/cvs423 Publication Date: 2013-01-22T01:20:43Z
ABSTRACT
In this study, we investigated the interaction between exercise-induced mitochondrial adaptation of large vessels and effects chronic anabolic androgenic steroids (AASs). Four groups Sprague–Dawley rats were studied: (i) sedentary, (ii) sedentary + nandrolone-treated, (iii) aerobic exercise trained, (iv) trained nandrolone-treated. Aerobic training increased levels aortic endothelial nitric oxide synthase (eNOS) heme oxygenase-1 (HO-1) in accordance with improved acetylcholine-induced vascular relaxation. These beneficial associated induction complexes I V, DNA copy number, greater expression transcription factors involved biogenesis/fusion. We also observed enhanced autophagy pathway activity, including conversion LC3-I to LC3-II beclin1 autophagy-related protein-7 (ATG7). The thiobarbituric acid-reactive substances protein carbonyls remained unchanged, whereas significant increases catalase manganese superoxide dismutase (MnSOD) aortas animals, when compared controls. Nandrolone oxidative stress biomarkers inhibited eNOS, HO-1, catalase, MnSOD expression. addition, it attenuated elevated peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) mitofusin-2 expression, further up-regulated LC3II conversion, beclin1, ATG7, dynamin-related protein-1 results demonstrate that nandrolone attenuates adaptations by regulating dynamic remodelling, down-regulation biogenesis intensive autophagy.
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