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Studies indicate that the anabolic nandrolone decanoate (Deca-Durabolin(r)) can modulate cell cycle regulation, but little is known about its effects on muscle cells. We have previously demonstrated that (a) deca-Durabolin(r)-induced inhibition of UCP1 cell proliferation was blocked in the presence of (b) (1) LPS; (c) (2) BMP1 agonists; (d) (3) E2/E1 (S(H)-4,9-dihydroxyphenyl)-N-ethyl-4,5-diphenyl-l-cysteinyl-methanol; and (e) (4) anti-proliferative agents. Here, we examined whether deca-Durabolin(r) modifies the expression of (a) UCP1 and (b) AMPK phosphorylation and (c) the expression of (d) MMP-2, muscle build up steroids. We analyzed (a) the expression of UCP1, both in whole tissues and in the striatum, and (b) AMPK phosphorylation in whole tissues. In (c) whole tissues, we used a panel of UCP1 immunolabeling sites (for UCP1, EZG, PDB1, PDB3, and PI, respectively) along with a cAMP-responsive element (CRE) site, high needs baby autism. In (d) and (e) striatum, we monitored the level of AMPK in individual neurons to determine if the AMPK-mediated inhibition of UCP1 by deca-Durabolin(r) is responsible for the increased levels of (d) MMP-2, or if the AMPK-mediated inhibition of (d) MMP-2 is responsible for the increased levels of (e) AMPK, androgenic steroids chemistry. For (c) whole striatum, we used a panel of UCP1 (EZG, PDB1, and PDB3) and AMPK (G2). The AMPK-induced inhibition of the UCP1 promoter was abolished by E2/E1 (S(H)-4,9-dihydroxyphenyl)-3-Methylphenol (SDPPM). Conversely, the AMPK-mediated inhibition of the UCP1 promoter was significantly enhanced by anti-proliferative agents (SDPPM), nandrolone decanoate studies. The inhibition of the UCP1 promoter by E2/E1 was blocked by E2/E1 (SDPPM) but not by anti-proliferative agents, nandrolone decanoate studies.
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