抗风湿金化合物对佛波酯诱导的核因子κB核转位以及一氧化氮和前列腺素E2生成的抑制作用

Inhibition of TPA-induced NF-kappaB nuclear translocation and production of NO and PGE2 by the anti-rheumatic gold compounds.

作者信息

Yamashita Masamichi, Ashino Shigeru, Oshima Yuko, Kawamura Shunsuke, Ohuchi Kazuo, Takayanagi Motoaki

机构信息

Department of Pathophysiological Science, Tohoku Pharmaceutical University, 4-4-1 Komatsushima, Aoba-ku, Sendai, Miyagi 981-8558, Japan.

出版信息

J Pharm Pharmacol. 2003 Feb;55(2):245-51. doi: 10.1211/002235702513.

DOI:10.1211/002235702513

PMID:12631417

Abstract

Auranofin, aurothioglucose and aurothiomalate (10 microM each) inhibited 12-O-tetradecanoylphorbol 13-acetate (TPA, 16.2 nM)-induced nuclear translocation of nuclear factor-kappa B (NF-kappaB), and production of nitric oxide (NO) and prostaglandin E(2) (PGE(2)) in rat peritoneal macrophages when the cells were pre-incubated with each gold compound for 20 h. Without pre-incubation for 20 h, aurothioglucose and aurothiomalate, but not auranofin, failed to inhibit the TPA-induced NF-kappaB nuclear translocation and production of NO and PGE(2). Auranofin, aurothioglucose and aurothiomalate did not affect the direct binding of NF-kappaB to the DNA probe. It was suggested that these gold compounds inhibit the TPA-induced production of NO and PGE(2) by inhibiting the NF-kappaB nuclear translocation.

摘要

当大鼠腹腔巨噬细胞与每种金化合物预孵育20小时后，金诺芬、硫代葡萄糖金和硫代苹果酸金（每种10微摩尔）抑制了12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯（TPA，16.2纳摩尔）诱导的核因子 - κB（NF - κB）核转位以及一氧化氮（NO）和前列腺素E2（PGE2）的产生。若不进行20小时的预孵育，硫代葡萄糖金和硫代苹果酸金，但金诺芬不抑制TPA诱导的NF - κB核转位以及NO和PGE2的产生。金诺芬、硫代葡萄糖金和硫代苹果酸金不影响NF - κB与DNA探针的直接结合。提示这些金化合物通过抑制NF - κB核转位来抑制TPA诱导的NO和PGE2的产生。