前列腺素E2
前列腺素E
信使核糖核酸
前列腺素
三氯生
肿瘤坏死因子α
微粒体
染色体易位
化学
细胞因子
酶
放射免疫分析
环氧合酶
分子生物学
内分泌学
内科学
生物
生物化学
医学
基因
病理
作者
Manal Mustafa,Biniyam Wondimu,Tülay Yucel‐Lindberg,A. T. Kats‐Hallström,Anita Jönsson,Thomas Modéer
标识
DOI:10.1111/j.1600-051x.2004.00622.x
摘要
Abstract Objective: The effect of triclosan (2,4,4′‐trichloro‐2′‐hydroxydiphenyl ether) on the expression of cyclooxygenase‐2 (COX‐2) and microsomal prostaglandin E synthase‐1 (mPGES‐1) and on the translocation of the nuclear factor‐ κ B (NF‐ κ B) in relation to prostaglandin E 2 (PGE 2 ) production was investigated in human gingival fibroblasts challenged with tumor necrosis factor α (TNF α ). Methods: Fibroblasts were established from gingival biopsies obtained from six children. COX‐2 mRNA and protein expression was quantified using mRNA quantitation and enzyme immunometric assay kits. mPGES‐1 mRNA was analysed by RT‐PCR, mPGES‐1 protein and NF‐κB translocation by immunoblotting. PGE 2 was determined by radioimmunoassay. Results: The cytokine TNF α enhanced the expression of mRNA as well as the protein levels of both COX‐2 and mPGES‐1 and subsequently the production of PGE 2 in gingival fibroblasts. Treatment of gingival fibroblasts with triclosan (1 μ g/ml) significantly reduced the stimulatory effect of TNF α (10 ng/ml) on the expression of mPGES‐1 at both the mRNA and the protein level by an average of 21% and 43%, respectively, and subsequently the production of PGE 2 ( p <0.01). Triclosan did not, however, affect the translocation of NF‐ κ B or the expression of COX‐2 in TNF α‐ stimulated cells. Conclusion: The results show that triclosan reduces the augmented biosynthesis of PGE 2 by inhibiting the mRNA and the protein expression of mPGES‐1 in gingival fibroblasts. This finding may partly explain the anti‐inflammatory effect of the agent previously reported in clinical studies.
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