Curcumina atenua as alterações patológicas dos músculos distróficos
China – esta pesquisa será apresentada no Encontro Anual da Sociedade Americana de Biologia Celular em dezembro. A curcumina é conhecida também como açafrão, um aditivo acrescentado na alimentação. A curcumina inibe a ativaçãoa da NF-kB que contribui para a degeneração muscular. Os animais tratados com curcumina apresentaram menor lesão muscular, além da redução da enzima CK, do fator de necrose tumoral, da interleucina 1 beta e da oxido nítrico sintetase induzida. O resumo em inglês da pesquisa pode ser lida abaixo:
Curcumin Attenuates Dystrophic Pathology in mdx Mice through Inhibiting NF-κB Activation
M. S. Zhu, C. Chen, Y. L. Hu, S. Chen – China
The dystrophin-glycoprotein complex has emerged as a scaffold responsible for the membrane docking of signaling proteins. There is no definitive cure available currently. In dystrophin-deficient muscular dystrophy, abnormal activation of signal pathways may play important roles in dystrophic pathogenesis. In this report, we found a natural botanical gradient, curcumin, capable of attenuating dystrophic pathology significantly and the mechanism underlying was involved in NF-κB inhibition. After treating X-linked muscular dystrophy (mdx) mice with 1 to 10 mg of curcumin, the sarcolemmic integrity assessed by Evans blue staining and muscle strength determined both by grip strength test and traction test were improved significantly. Histological analysis demonstrated that curcumin reduced severity of myofibril necrosis and extent of regenerating fibers as well as the variability in size of fibers. Creatine kinase level and the expressions of tumor necrosis factor alpha, interleukine-1 beta and inducible nitric oxide synthase were decreased also after curcumin treatment. Consistently, elevated NF-κB activity in muscle fibers of mdx mice decreased after curcumin administration. Since curcumin is a non-toxic compound derived from C.longa, which was widely used in healthy food. The possible effect of curcumin may be worth studying in Duchenne muscular dystrophy therapy.
(46th Annual Meeting American Society for Cell Biology – San Diego, December 2006)
