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Inducible nitric oxide synthase contributes to gender differences in ischemic brain injury

Title
Inducible nitric oxide synthase contributes to gender differences in ischemic brain injury
Authors
Park E.-M.Cho S.Frys K.A.Glickstein S.B.Zhou P.Anrather J.Ross M.E.Iadecola C.
Ewha Authors
박은미
SCOPUS Author ID
박은미scopus
Issue Date
2006
Journal Title
Journal of Cerebral Blood Flow and Metabolism
ISSN
0271-678XJCR Link
Citation
vol. 26, no. 3, pp. 392 - 401
Indexed
SCI; SCIE; SCOPUS scopus
Abstract
Estrogens have antiinflammatory actions and protect the brain from ischemic injury. Cerebral ischemia is accompanied by an inflammatory reaction that contributes to the tissue damage, an effect mediated in part by toxic amounts of nitric oxide (NO) produced by the inducible isoform of NO synthase (iNOS). Therefore, estrogens may protect the female brain by modulating postischemic iNOS expression. To test this hypothesis, we studied whether iNOS plays a role in the mechanisms of the reduced susceptibility to ischemic injury observed in female mice. The middle cerebral artery was occluded for 20 mins using an intraluminal filament in C57BI/6 mice, and infarct volume was assessed 3 days later in cresyl violet-stained sections. Infarcts were 53% smaller in female mice than in males (P < 0.05), a reduction abolished by ovariectomy (OVX) and reinstated by estrogen replacement. In normal female mice, postischemic iNOS mRNA was lower than in males (P < 0.05). Ovariectomy increased iNOS mRNA after ischemia and estrogen replacement blocked this effect. Furthermore, the iNOS inhibitor aminoguanidine reduced infarct volume in male, but not in female, mice. Similarly, male iNOS-null mice had smaller infarcts than wild-type mice, but female iNOS nulls were not protected. Ovariectomy and OVX with estrogen replacement did not affect infarct volume in iNOS-null female mice. The findings suggest that the neuroprotection conferred by estrogens is, in part, related to attenuation of iNOS expression. Such attenuation could result from the potent antiinflammatory effects of estrogens that downregulate iNOS expression via transcriptional or posttranscriptional mechanisms. © 2006 ISCBFM All rights reserved.
DOI
10.1038/sj.jcbfm.9600194
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
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