作者: Yong-Fei Zhao , Xiang Zhang , Zhi-Bin Ding , Xing-Wang Yang , Hui Zhang
DOI: 10.1007/S12031-014-0411-7
关键词:
摘要: Although therapeutic potential of fasudil in EAE is promising, action mechanism and clinical limitations are still not fully understood resolved. In this study, we observed the a novel Rho kinase (ROCK) inhibitor FaD-1, derivative, explored possible MOG35-55-induced EAE. Experimental autoimmune encephalomyelitis (EAE) was induced by myelin oligodendrocyte glycoprotein (MOG35-55) immunization. The pathology spinal cord measured immunohistochemistry neurological impairment evaluated using scores. as ROCK inhibitor, inhibited expression II that mainly expressed CNS. We show here FaD-1 ameliorates defects severity MOG-induced mice, accompanied protection demyelination inhibition neuroinflammation addition, dampened TLR2 TLR4 signaling well Th1 (IFN-γ) Th17 (IL-17) responses also prevented iNOS production inflammatory cytokine IL-1β, IL-6, TNF-α which specific markers for M1 microglia/macrophages. This study highlights treatment human diseases with both components.