Tolman E L, Fuller B L, Rosenthale M E
Prostaglandins Leukot Med. 1985 Jun;18(3):367-77. doi: 10.1016/0262-1746(85)90070-8.
Suprofen is a non-narcotic, peripheral analgesic that exhibits potent prostaglandin (PG) synthesis inhibitory activities in a variety of subcellular tissue preparations and in vivo. The results of the present study show suprofen to be significantly more potent than either ibuprofen (6-fold) or aspirin (1000-fold) as an inhibitor of PG production by cell-free preparations of guinea pig uteri. It is selectively more potent against the production of PGF2 alpha and PGE2 than against the formation of 6-keto PGF1 alpha, the stable metabolite of prostacyclin. Suprofen is markedly more potent inhibiting the conversion of arachidonic acid to PGF2 alpha than is ibuprofen (30 times) or aspirin (1250 times). Taken together with the important role PGF2 alpha plays in the etiology of dysmenorrhea and the observation (Hahn et al., 1982) that suprofen is more potent and effective than a number of other PG synthesis inhibitors, including ibuprofen and aspirin, at reducing in vivo guinea pig uterine contractions induced by arachidonic acid, the results of the present study suggest a mechanism to support the clinical findings that suprofen is a very effective treatment for the signs and symptoms of dysmenorrhea.
舒洛芬是一种非麻醉性外周镇痛药，在多种亚细胞组织制剂和体内均表现出强大的前列腺素（PG）合成抑制活性。本研究结果表明，作为豚鼠子宫无细胞制剂中PG生成的抑制剂，舒洛芬的效力明显高于布洛芬（6倍）或阿司匹林（1000倍）。它对PGF2α和PGE2生成的选择性抑制作用比对前列环素的稳定代谢产物6-酮-PGF1α的生成更强。舒洛芬抑制花生四烯酸转化为PGF2α的效力明显高于布洛芬（30倍）或阿司匹林（1250倍）。鉴于PGF2α在痛经病因中起重要作用，以及观察到（哈恩等人，1982年）舒洛芬在减少花生四烯酸诱导的豚鼠子宫体内收缩方面比包括布洛芬和阿司匹林在内的许多其他PG合成抑制剂更有效，本研究结果提示了一种机制来支持舒洛芬是痛经症状非常有效治疗方法的临床发现。
