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Am J Physiol Heart Circ Physiol 286: H2010-H2019, 2004. First published December 18, 2003; doi:10.1152/ajpheart.00481.2003
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Estrogen suppresses IL-1{beta}-mediated induction of COX-2 pathway in rat cerebral blood vessels

Jose A. Ospina, Holly N. Brevig, Diana N. Krause, and Sue P. Duckles

Department of Pharmacology, College of Medicine, University of California, Irvine, California 92697-4625

Submitted 27 May 2003 ; accepted in final form 10 December 2003

Interleukin (IL)-1{beta} is a potent inducer of inflammatory prostaglandins, which are important mediators of vascular response to cerebral injury, whereas estrogen reduces brain injury in models of ischemic stroke. Thus we examined the 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 nontreated ovariectomized female rats received IL-1{beta} injections (10 µg/kg ip), and then cerebral vessels were isolated for biochemical and contractile measurements. In estrogen-deficient rats, IL-1{beta} induced cerebrovascular COX-2 protein expression; a peak response occurred 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 as measured in isolated cerebral arteries; the latter effect was partially reversed by treatment with the selective COX-2 inhibitor NS-398 (10 µmol/l). 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 the nuclear factor-{kappa}B inhibitor caffeic acid phenethyl ester (20 mg/kg ip), and estrogen treatment reduced cerebrovascular nuclear factor-{kappa}B activity. Estrogen thus has potent anti-inflammatory effects with respect to cerebral vascular responses to IL-1{beta}. These effects may have important implications for the incidence and severity of cerebrovascular disease.

17{beta}-estradiol; cyclooxygenase-2; prostaglandin E2; nuclear factor-{kappa}B; interleukin-1{beta}


Address for reprint requests and other correspondence: S. P. Duckles, Dept. of Pharmacology, College of Medicine, Univ. of California, Irvine, CA 92697-4625 (E-mail: spduckle{at}uci.edu).




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