Ex?vivo study.
University hospital.
Fifteen premenopausal patients undergoing surgery for benign gynecologic disorders.
Endometrial explants were obtained by aspiration curettage and stimulated ex?vivo with interleukin-1¦Â before exposure to CMA or DEX; mRNA levels were determined via reverse transcription-quantitative real-time polymerase chain reaction, and concentrations of arachidonic acid metabolites by enzyme immunoassays.
Messenger RNA levels of COX-2, ANXA1, PR, and GR; concentrations of PGF2¦Á, LTB4, and LTC4 in endometrial explants treated with CMA or DEX.
In IL-1¦Â-treated explants COX-2 mRNA and PGF2¦Á, concentrations were significantly down-regulated by CMA but not by DEX. Chlormadinone acetate 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.