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Am J Physiol Heart Circ Physiol (December 18, 2003). doi:10.1152/ajpheart.00481.2003
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Submitted on May 27, 2003
Accepted on December 10, 2003

Estrogen suppresses IL-1{beta}-mediated induction of the cyclooxygenase-2 pathway in rat cerebral blood vessels

Jose A. Ospina1, Holly N. Brevig1, Diana N. Krause1, and Sue P. Duckles1*

1 Department of Pharmacology, University of California, College of Medicine, Irvine, CA, USA

* To whom correspondence should be addressed. E-mail: spduckle{at}uci.edu.

IL-1{beta} is a potent inducer of inflammatory prostaglandins (PG) which are important mediators of the vascular response to cerebral injury, whereas estrogen reduces brain injury in models of ischemic stroke. Thus we examined effects of in vivo IL-1{beta} exposure on cerebrovascular cyclooxygenase (COX)-2 expression and function in an animal model of chronic estrogen replacement. Estrogen-treated and non-treated ovariectomized female rats received intraperitoneal IL-1{beta} injections (10 µg/kg), and then cerebral vessels were isolated for biochemical and contractile measurements. In estrogen-deficient rats, IL-1{beta} induced cerebrovascular COX-2 protein expression with a peak response occurring 3 h after injection. COX-2 was localized to arterial endothelium using confocal microscopy. IL-1{beta} increased PGE2, but not PGI2, production and decreased vascular tone measured in isolated cerebral arteries; the latter effect was partially reversed by treatment with a selective COX-2 inhibitor (10 µmol/L NS-398). In contrast, in animals treated with estrogen, IL-1{beta} had no significant effect on COX-2 protein levels, PGE2 production, or vascular tone. Combined treatment with 17{beta}-estradiol and medroxyprogesterone acetate also prevented increases in PGE2 production after IL-1{beta} treatment, but treatment with 17{alpha}-estradiol had no effect. IL-1{beta} induction of COX-2 protein was prevented by treatment with an NF-{kappa}B inhibitor (caffeic acid phenethyl ester; 20 mg/kg, i.p.), and estrogen treatment reduced cerebrovascular NF-{kappa}B activity. Estrogen thus has potent anti-inflammatory effects with respect to the cerebral vascular response to IL-1{beta}. These effects may have important implications for the incidence and severity of cerebrovascular disease.




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