期刊
BRAIN RESEARCH
卷 1008, 期 2, 页码 147-154出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.brainres.2004.02.019
关键词
stroke; estrogen; NF kappa B; neuroprotection; post-ischemic inflammation
资金
- NIA NIH HHS [AG10485, AG22550, P01 AG022550, P01 AG010485] Funding Source: Medline
The protective effects of estrogens have been widely reported in a number of animal and cell culture models, but the molecular mechanisms of this potent neuroprotective activity are not well understood. Both in vitro and in vivo studies indicate that in the central nervous system and peripheral tissues, estrogen treatment reduces cytokine production and inflammatory responses. Nuclear factor-kappa B (NFkappaB) plays an essential role in the regulation of post-ischemic inflammation, which is detrimental to recovery from an ischemic stroke. We investigated the role of NFkappaB in neuronal survival in rats that received transient middle cerebral artery (MCA) occlusion, and observed that this transient cerebral ischemia induced substantial apoptosis and inflammatory responses, including IkappaB phosphotylation, NF-kappaB activation and iNOs over-expression. 17 beta-estradio1 (E2) treatment produced strong protective effects by reducing infarct volume neuronal apoptosis and inflamtnatoty responses. These findings provide evidence for a novel molecular and cellular interaction between the sex hormone and the immunoresponsive system. These studies also provide evidence that suppression of post-ischemic inflammation may play a critical role in estrogen-mediated neuroprotection. (C) 2004 Elsevier B.V. All rights reserved.
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