Aida Hanjalic-Beck, M.D., Wolfgang R. Schäfer, Ph.D., Wolfgang R. Deppert, Ph.D., Lara Fischer, Antonia Stein, Laura Seebacher, M.D., Akou Seli von Gradowski, Johanna Stuckenschneider, Hans P. Zahradnik, M.D.
Vol 98, Issue 4, Pages 1017-1022
To elucidate the mode of action of chlormadinone acetate (CMA) in reducing dysmenorrheic pain, we studied the effects of CMA and dexamethasone (DEX) on mRNA abundance of cyclooxygenase-2 (COX-2), annexin-1 (ANXA1), glucocorticoid receptor (GR), progesterone receptor (PR) and concentrations of prostaglandin F2α (PGF2α) and leukotrienes B4 (LTB4) and C4 (LTC4) in human endometrial explants.
Ex vivo study.
Fifteen premenopausal patients undergoing surgery for benign gynaecological disorders.
Endometrial explants were obtained by aspiration curettage and stimulated ex vivo with IL-1β before exposure to CMA or DEX, mRNA levels were determined via reverse transcription quantitative real-time PCR (RT-qPCR) and concentrations of arachidonic acid metabolites by enzyme immunoassays.
Main Outcome Measures:
Messenger RNA levels of COX-2, ANXA1, PR, and GR; concentrations of PGF2α, LTB4, and LTC4 in endometrial explants treated with CMA or DEX.
In IL-1ß-treated explants COX-2 mRNA and PGF2α concentrations were significantly down-regulated by CMA, but not by DEX. CMA did not affect mRNA abundance of ANXA1, PR and GR.
Our data suggest that CMA is a suppressor of COX-2 expression. Comparison with DEX revealed that progestin specific activity of CMA may mainly be responsible for suppression of prostaglandin biosynthesis in human endometrium.
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