Tsang B K, Ooi T C
Am J Obstet Gynecol. 1982 Mar 15;142(6 Pt 1):626-33. doi: 10.1016/s0002-9378(16)32431-0.
Late proliferative (days 9 to 14) and midsecretory (days 18 to 24) human endometria were maintained in organ culture in the presence of 17 beta-estradiol and/or progesterone or mefenamic acid 17 beta-estradiol (0.1 to 1,000 ng/ml) increased prostaglandin F (PGF) secretion by both proliferative and secretory endometria. Progesterone (1,000 ng/ml) markedly inhibited PGF secretion by proliferative but not secretory endometrium. 17 beta-estradiol and progesterone had no effect on prostaglandin E (PGE) secretion by both types of endometrium. Secretion of both PGF and PGE by proliferative and secretory endometria was inhibited by mefenamic acid ( 1 microgram/ml). This was more apparent with PGF secretion and was detectable within the first 2 hours of culture. These findings indicate that the human endometrium is a rich source of PGF and PGE and that the production of PGF is regulated by gonadal steroids. These results support the concept that one mechanism of action of mefenamic acid in the treatment of dysmenorrhea is inhibition of prostaglandin production.
将增殖晚期（第9至14天）和分泌中期（第18至24天）的人子宫内膜在含有17β-雌二醇和/或孕酮或甲芬那酸的条件下进行器官培养。17β-雌二醇（0.1至1000 ng/ml）可增加增殖期和分泌期子宫内膜的前列腺素F（PGF）分泌。孕酮（1000 ng/ml）显著抑制增殖期子宫内膜的PGF分泌，但对分泌期子宫内膜无此作用。17β-雌二醇和孕酮对两种类型子宫内膜的前列腺素E（PGE）分泌均无影响。甲芬那酸（1微克/毫升）可抑制增殖期和分泌期子宫内膜的PGF和PGE分泌。这在PGF分泌方面更为明显，且在培养的最初2小时内即可检测到。这些发现表明，人子宫内膜是PGF和PGE的丰富来源，且PGF的产生受性腺类固醇调节。这些结果支持了甲芬那酸治疗痛经的作用机制之一是抑制前列腺素产生这一概念。
