Nitric oxide-mediated neuronal injury in multiple sclerosis
作者： M.P. Sherman , J.M. Griscavage , L.J. Ignarro
DOI: 10.1016/0306-9877(92)90175-C
关键词:
摘要: Although several explanations have been proposed for destruction of myelin and oligodendrocytes in multiple sclerosis, there is no proven mechanism injury. We postulate that the autoimmune response seen sclerosis results a cytokine-mediated increase nitric oxide production by macrophages/microglia, smooth muscle cells and/or endothelium central nervous system. 3 mechanisms cellular damage due to are proposed: 1. direct cytotoxicity; 2. injury peroxynitrite formation from superoxide anion oxide; 3. oxide-mediated elevations cGMP enhance tumor necrosis factor-alpha toxicity. In support these hypotheses, anti-inflammatory effectors, dexamethasone transforming growth factor-beta, ameliorate symptoms clinical experimental allergic encephalitis, respectively. These 2 immunomodulators also inhibit induction macrophages. An design therapeutic interventions which will evaluate role pathophysiology encephalitis presented.
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