ElAttar T M, Lin H S
Laboratory of Hormone Research, University of Missouri-Kansas City School of Dentistry, Missouri 64108.
Prostaglandins Leukot Essent Fatty Acids. 1991 Jul;43(3):175-8. doi: 10.1016/0952-3278(91)90165-2.
Several studies have correlated the excessive production of prostaglandins (PGs) with tumor promotion and the suppression of the immune response. Inhibition of PGs by pharmacological agents has been demonstrated to enhance immunocompetence, and to suppress growth of tumors in animals and humans. In this study we examined the effect of retinol (I), all-trans-retinoic acid (II), N-(4-Hydroxyphenyl) retinamide (N-4-HPR) (III), canthaxanthin (CTX) (IV), and beta-carotene (beta-CT) (V) on the bioconversion of 14C-arachidonic acid (AA) to PGE2 by squamous carcinoma cells of the tongue, SCC-25. Agents (I), (II), (III), (IV) inhibited while (V) stimulated PGE2 formation in a dose related manner. N-4-HPR was the most potent inhibitor of PGE2 synthesis. The data suggest that certain retinoids and carotenoids have the potential of inhibition of PG synthesis by oral squamous carcinoma cells. Inhibitory effects such as those described here and antioxidant properties might in part contribute to the antiinflammatory and anticarcinogenic activity of retinoids in vivo.
多项研究已将前列腺素（PGs）的过度产生与肿瘤促进及免疫反应抑制联系起来。药理学试剂对PGs的抑制已被证明可增强免疫能力，并抑制动物和人类肿瘤的生长。在本研究中，我们检测了视黄醇（I）、全反式维甲酸（II）、N-（4-羟基苯基）视黄酰胺（N-4-HPR）（III）、角黄素（CTX）（IV）和β-胡萝卜素（β-CT）（V）对舌鳞状癌细胞SCC-25将14C-花生四烯酸（AA）生物转化为PGE2的影响。试剂（I）、（II）、（III）、（IV）呈剂量相关方式抑制，而（V）刺激PGE2的形成。N-4-HPR是PGE2合成的最有效抑制剂。数据表明某些类视黄醇和类胡萝卜素具有抑制口腔鳞状癌细胞合成PG的潜力。此处所述的抑制作用以及抗氧化特性可能部分有助于类视黄醇在体内的抗炎和抗癌活性。
