Abstract
We investigated the regulation of cyclooxygenase-2 (COX-2) by 17-β-estradiol (E 2) in the rat oviduct. We observed that COX-2 is expressed mainly in proestrous and estrous stages, periods under estrogenic influence. While exogenous administration of E 2 (1 μg/rat) significantly increased COX-2 protein levels, progesterone did not modify it. COX-2 was mainly localized on oviductal epithelial cells from estrogenized rat. Induction of COX-2 expression by E 2 was partially reverted by tamoxifen (1 mg/rat), an E 2 receptor antagonist. Estradiol treatment also increased prostaglandins (PGs) synthesis: 6-keto-PGF 1α (40%), a stable metabolite of prostacyclin (PGI 2), PGF 2α (40%) and PGE 2 (50%). Tamoxifen completely suppressed this enhancement. In order to discriminate which isoform of COX was implicated in the stimulatory effect of E 2 on PGs synthesis, oviducts were preincubated with meloxicam (Melo: 10 −9 M) or NS-398 (10 −7 M), two selective COX-2 inhibitors. Both Melo and NS-398 abolished the increase of PGs synthesis stimulated by E 2. All together, these data indicate that E 2 could upregulate COX-2 expression and activity in the rat oviduct and that the stimulatory effect of E 2 may be receptor-mediated.
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