VanLandingham Jacob W, Cekic Milos, Cutler Sarah, Hoffman Stuart W, Stein Donald G
Department of Emergency Medicine, Emory University, Atlanta, GA, USA.
Neurosci Lett. 2007 Sep 25;425(2):94-8. doi: 10.1016/j.neulet.2007.08.045. Epub 2007 Aug 25.
The inflammatory cascade that follows traumatic brain injury may lead to secondary cell death and can impede recovery of function. Complement factors and their convertases are increased in glia after brain injury and lead to the production of inflammatory products that kill vulnerable neurons. Progesterone and its metabolite allopregnanolone (5alpha-pregnan-3beta-ol-20-one) have been shown to reduce the expression of inflammatory cytokines in the acute stages of brain injury, although how they do this is not completely understood. In this study we show that both progesterone and allopregnanolone treatments enhance the production of CD55 following contusion injuries of the cerebral cortex in rats. CD55, a single-chain type 1 cell surface protein, is a potent inhibitor of the complement convertases which are activators of the inflammatory cascade. The increased expression of CD55 could be an important mechanism by which steroids help to reduce the cerebral damage caused by inflammation.
创伤性脑损伤后发生的炎症级联反应可能导致继发性细胞死亡，并会阻碍功能恢复。脑损伤后神经胶质细胞中的补体因子及其转化酶增加，导致产生杀死易损神经元的炎性产物。孕酮及其代谢产物别孕烯醇酮（5α-孕烷-3β-醇-20-酮）已被证明可在脑损伤急性期降低炎性细胞因子的表达，尽管其具体机制尚不完全清楚。在本研究中，我们发现孕酮和别孕烯醇酮处理均可增强大鼠大脑皮质挫伤损伤后CD55的产生。CD55是一种单链1型细胞表面蛋白，是炎性级联反应激活剂补体转化酶的有效抑制剂。CD55表达增加可能是类固醇有助于减轻炎症所致脑损伤的重要机制。
