Sulforafano melhora as alterações da distrofia muscular em camundongos

26 de dezembro de 2014 by Izabel Gavinho

China – O sulforafano é um produto antixoidante presente em alimentos . Os animais tratdos apresentaram aumento da força e da massa muscular, aumento da caminhada, com redução da CK e da DHL. Além disso os animais apresentaram hipertrofia muscular e cardíaca.

O resumo em inglês pode ser lido abaixo:

(J.Appl.Physiol, 2014) Sulforaphane alleviates muscular dystrophy in mdx mice by activation of Nrf2

Chengcao Sun, Cuili Yang, Ruilin Xue, Shujun Li, Ting Zhang, Lei Pan, Xuejiao Ma, Liang Wang, and Dejia Li – China
Sulforaphane (SFN), one of the most important isothiocyanates in the human diet, is known to have chemo-preventive and antioxidant activities in different tissues via activation of NF-E2-related factor 2 (Nrf2)-mediated induction of antioxidant/phase II enzymes, such as heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase 1 (NQO1). However, its effects on muscular dystrophy remain unknown. This work was undertaken to evaluate the effects of SFN on Duchenne muscular dystrophy (DMD). 4-week-old mdx mice were treated with SFN by gavage (2 mg/kg body weight per day for 8 weeks), and our results demonstrated that SFN treatment increased the expression and activity of muscle phase II enzymes NQO1 and HO-1 with Nrf2 dependent manner. SFN significantly increased skeletal muscle mass, muscle force (~30%), running distance (~20%) and GSH/GSSG ratio (~3.2 folds) of mdx mice, and decreased the activities of plasma creatine phosphokinase (CK) (~45%) and lactate dehydrogenase (LDH) (~40%), gastrocnemius hypertrophy (~25%), myocardial hypertrophy (~20%) and MDA levels (~60%). Further, SFN treatment also reduced the central nucleation (~40%), fiber size variability, inflammation and improved the sarcolemmal integrity of mdx mice. Collectively, these results show that SFN can improve muscle function, pathology and protect dystrophic muscle from oxidative damage in mdx mice through Nrf2 signaling pathway, which indicate Nrf2 may represent a new therapeutic target for muscular dystrophy.


Fonte: http://distrofiamuscular.net/principal.htm

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