Nova droga experimental é bem bons resultados em camundongos

Japão - a prostaglandina sintetase aumanta a necrose de fibras musculares na distrofia muscular de Duchenne; pesquisadores japoneses identificaram um nova droga, HQL-79, que inibe a prostaglandina sintetase. Estudando a droga dada por via oral por 5 dias em camundongos os autores observaram redução da necrose muscular e redução das citocinas inflamatórias, podendo ser útil para tratamento da distrofia muscular.

O resumo em inglês pode ser lido abaixo:

(FEBS Journal. 276 Suppl. 1:349, July 2009) Chemotherapy of Duchenne’s muscular dystrophy

Y. Urade, M. Hayashi, T. Maruyama, S. Kamauchi, I. Mohri and K. Aritake - Japan

Duchenne muscular dystrophy (DMD) is an X-linked muscular abnormality caused by the loss of dystrophin and is one of the most gravely genetic disorders. We have recently found that hematopoietic prostaglandin (PG) D synthase (H-PGDS) was induced in grouped necrotic muscle fibers in DMD patients (Okinaga T. et al., Acta Neuropathol. 2002; 104: 377–384). We developed novel H-PGDS inhibitors based on the X-ray crystallographic analysis of human H-PGDS complexed with its prototype inhibitor, HQL-79 (Aritake K. et al., J. Biol. Chem. 2006: 281: 15277–15286). In this study, we developed a novel therapy for DMD by inhibition of H-PGDS. H-PGDS was localized in the necrotic muscle fibers and accumulated macrophages in mdx mice. Oral administration of H-PGDS inhibitors for 5 days prevented the expansion of muscular necrosis in an mdx mouse model, as measured by X-ray computed tomography (CT) imaging enhanced by non-ionic contrast media. The treatment with H-PGDS inhibitors also decreased the expression of mRNAs of pro-inflammatory cytokines. These results indicate that PGD2 produced by H-PGDS plays important pathological roles on the expansion of muscle necrosis. H-PGDS inhibitor also accelerated the accumulation and activation of macrophages in the necrotic area. These results indicate that PGD2 produced by H-PGDS is involved in the expansion of muscle necrosis in DMD and that inhibition of H-PGDS is a novel therapy for DMD.

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