Key result
Nandrolone decanoate abolishes the exercise-induced MMP-2 increase in rat left ventricles, suggesting impaired cardiac remodeling.
Why the study?
The effects of nandrolone decanoate on MMP-2 activity and protein level in the left ventricle after mechanical load exercise were not well understood.
Does nandrolone decanoate inhibit MMP-2 activity in the left ventricle of exercised rats?
Does nandrolone decanoate inhibit MMP-2 activity in the left ventricle of exercised rats?
Nandrolone decanoate abolishes exercise-induced increases in MMP-2 activity and protein levels in the rat left ventricle, suggesting a mechanism for impaired cardiac tissue remodeling.
AAS abolished exercise-induced LV MMP-2 rise in rats; leaves open whether steroids impair human cardiac remodeling.
The indiscriminate use of anabolic-androgenic steroids has been shown to induce left ventricular dysfunctions. The main objective of the present study was to investigate the effects of nandrolone decanoate on matrix metalloprotease (MMP-2) activity and protein level in the left ventricle (LV) of rats after 7 weeks of mechanical load exercise. Wistar rats were grouped into: sedentary (S); nandrolone decanoate-treated sedentary (AAS); trained without AAS (T) and trained and treated with AAS (AAST). Exercised groups performed a 7-weeks water-jumping program. Training significantly increased the MMP-2 activity by zymography and the protein level by Western blotting analysis. However, the AAS treatment abolished both the increase in MMP activity and protein level induced by exercise. These results suggest that AAS may impair cardiac tissue remodeling which may lead to the heart malfunction.
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Marqueti et al. (2012) studied Cardiac tissue remodeling. Nandrolone decanoate vs. No nandrolone decanoate (sedentary or trained) was evaluated on Matrix metalloprotease (MMP-2) activity and protein level in the left ventricle. Nandrolone decanoate treatment abolished the exercise-induced increase in MMP-2 activity and protein level in the left ventricle of rats, suggesting impaired cardiac tissue remodeling.
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