Wood P L
CoCensys Inc., Irvine, CA 92718, USA.
Neurol Res. 1995 Aug;17(4):242-8. doi: 10.1080/01616412.1995.11740321.
The sequalae evoked by an initial ischemic event in the CNS are incredibly complex and involve a wide range of short-term and long-term metabolic adaptations. With regard to the 'penumbra' area, in which cell death occurs over a 1 to 3 day period, defining the roles of potential neurotoxic mediators is crucial. In this regard, upon cellular activation after an ischemic episode, microglia, the resident macrophages of the CNS, can produce large quantities of a number of neurotoxic mediators. These factors include excitatory amino acids, proteases, cytokinases and nitric oxides. In this manuscript, these mediators are reviewed with regard to the potential utility of suppression of microglial function, via immunosuppressive agents, in the treatment of stroke.
中枢神经系统初次缺血事件引发的后遗症极其复杂，涉及广泛的短期和长期代谢适应。对于在1至3天内发生细胞死亡的“半暗带”区域而言，明确潜在神经毒性介质的作用至关重要。在这方面，缺血发作后细胞激活时，中枢神经系统的常驻巨噬细胞——小胶质细胞可产生大量多种神经毒性介质。这些因素包括兴奋性氨基酸、蛋白酶、细胞激酶和一氧化氮。在本手稿中，将针对通过免疫抑制剂抑制小胶质细胞功能在中风治疗中的潜在效用对这些介质进行综述。
