Autor(es): Pineda Arnold Angelo M.; Minohara Motozumi; Kawamura Nobutoshi; Matsushita Takuya; Yamasaki Ryo; Sun Xiaojia; Piao Hua; Shimokawa Hiroaki; Kira Jun-ichi

Resumo: We studied the effects of fasudil, a selective Rho-kinase inhibitor, on experimental autoimmune neuritis (EAN). Continuous parenteral administration of fasudil prevented the development of EAN induced by P0 peptide 180-199 in Lewis rats while it also reduced EAN severity when administered after disease onset. Immunohistochemical examination disclosed a marked decrease in the amount of inflammatory cell infiltration and attenuation of demyelination and axonal degeneration. Specific proliferation of lymphocytes from fasudil-treated rats in response to P0 peptide was significantly reduced as compared with those from phosphate-buffered saline (PBS)-treated rats. Fasudil treatment was associated with a significant reduction in secretion of IFN-?; by contrast, secretion of IL-4 was almost the same in the fasudil- and PBS-treated groups. As a result, the IFN-?/IL-4 ratio in the supernatant was significantly deceased in fasudil-treated rats compared with PBS-treated ones. Therefore, our results indicate a beneficial effect of selective blockade of Rho-kinase in animals with autoimmune inflammation of the peripheral nerves, and may provide a rationale for the selective blockade of Rho-kinase as a new therapy for Guillain-Barré syndrome.

Imprenta: Journal of the Neurological Sciences, v. 306, n. 1-2, p. 115-120, 2011

Identificador do objeto digital: 10.1016/j.jns.2011.03.031

Descritores: Guillain-Barre Syndrome - Biosynthesis ; Guillain-Barre Syndrome - Cell ; Guillain-Barre Syndrome - Cytopathology ; Guillain-Barre Syndrome - Pathogenesis ; Guillain-Barre Syndrome - Proteins ; Guillain-Barre Syndrome - Cytokines ; Guillain-Barre Syndrome - Inflammation ; Guillain-Barre Syndrome - Immunology

Data de publicação: 2011

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