J Korean Acad Periodontol.  2004 Jun;34(2):345-356. 10.5051/jkape.2004.34.2.345.

Triclosan Inhibition of Prostaglandin E2 Production in Human Gingival Fibroblast

• Park SP
• Chung HJ
• Kim YJ
• Kim OS

• KMID: 2045159
• DOI: http://doi.org/10.5051/jkape.2004.34.2.345

Abstract

The triclosan was shown to have anti-microbial and anti-inflammatory effect with inhibition of inflammatory mediators such as prostaglandin E2 (PGE2). The purpose of this study was to elucidate whether and how PGE2 could be inhibited by triclosan in human gingival fibroblast. Human gingival fibroblast-1 cells (ATCC CRL2014) were pre-treated for 1 hour with triclosan (0.001 microgram/ml~ 10 microgram/ml) and then stimulated with TNF-alpha(1.0 ng/ml). PGE2 synthesis was evaluated by ELISA and gene expression of COX-1 and COX-2 was evaluated by RT-PCR after TNF-alpha, triclosan, and NS-398 (COX-2 inhibitor, 5 micrometer) and/ or cycloheximide (protein synthesis inhibitor, 2 microgram/ml). Triclosan was cytotoxic to human gingival fibroblasts in the concentration higher than 1.0 microgram/ml for longer than 24 hours in tissue culture. The PGE2 synthesis was inhibited by triclosan in dose-dependent manner. Greater COX-2 mRNA suppression was observed with triclosan (0.1 microgram/ml) than with TNF-alphaalone, without change in COX-1 gene expression. Inhibitory effects of triclosan on PGE2 synthesis disappeared in presence of cycloheximide. This study suggests that triclosan inhibit prostaglandin E2 at the level of COX-2 gene regulation and require de novo protein synthesis.

Keyword

triclosan; prostaglandin E2; COX-1; COX-2; human gingival fibroblast; RT-PCR

MeSH Terms

Cycloheximide
Dinoprostone*
Enzyme-Linked Immunosorbent Assay
Fibroblasts*
Gene Expression
Humans*
RNA, Messenger
Triclosan*
Tumor Necrosis Factor-alpha
Cycloheximide
Dinoprostone
RNA, Messenger
Triclosan
Tumor Necrosis Factor-alpha