期刊
NEUROSCIENCE LETTERS
卷 425, 期 2, 页码 94-98出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2007.08.045
关键词
traumatic brain injury; progesterone; allopregnanolone CD55; inflammation
资金
- NIGMS NIH HHS [T32 GM008169] Funding Source: Medline
- NINDS NIH HHS [R01 NS048451-02, R01 NS048451-03S1, R01 NS048451-01A2, R01 NS048451, R01 NS048451-03] Funding Source: Medline
- PHS HHS [R01N538664, R01N540825] Funding Source: Medline
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 (5 alpha-pregnan-3 beta-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. (c) 2007 Elsevier Ireland Ltd. All rights reserved.
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