Inoue H, Kubota T, Ando K, Aihara M, Sozumi T, Ishida H
Department of Plastic and Reconstructive Surgery, St. Marianna University School of Medicine, Miyamae, Kawasaki, Japan.
Life Sci. 1997;61(12):PL 171-6. doi: 10.1016/s0024-3205(97)00663-2.
The effects of azelastine on prostaglandin E2 (PGE2) production were investigated by using cultured normal dermal fibroblasts obtained from the same traumatic region of 3 patients and the CRL-1475 cell line. Interleukin-1beta (IL-1) enhanced PGE2 production in cultured normal fibroblasts and CRL-1475 cells. 10(-6) M azelastine inhibited PGE2 production in these IL-1-stimulated fibroblasts. However, the drug did not influence spontaneous PGE2 production in cultured CRL-1475 fibroblasts not stimulated with IL-1 but slightly it increased in cultured normal dermal fibroblasts under the same conditions. These results suggest that azelastine either regulates synthesis of an inducible cyclooxygenose protein or inhibits PGE2 production as an inducible cyclooxygenase inhibitor.
采用从3例患者同一创伤部位获取的培养正常真皮成纤维细胞和CRL - 1475细胞系,研究了氮卓斯汀对前列腺素E2(PGE2)生成的影响。白细胞介素 - 1β(IL - 1)增强了培养的正常成纤维细胞和CRL - 1475细胞中PGE2的生成。10(-6)M氮卓斯汀抑制了这些IL - 1刺激的成纤维细胞中PGE2的生成。然而,该药物对未用IL - 1刺激的培养CRL - 1475成纤维细胞中PGE2的自发生成没有影响,但在相同条件下,培养的正常真皮成纤维细胞中PGE2的生成略有增加。这些结果表明,氮卓斯汀要么调节诱导型环氧化酶蛋白的合成,要么作为诱导型环氧化酶抑制剂抑制PGE2的生成。