Triptolide inhibits murine-inducible nitric oxide synthase expression by down-regulating lipopolysaccharide-induced activity of nuclear factor-kB and c-Jun NH2-terminal kinase
- Author(s)
- Young-Ho Kim; Sang-Han Lee; Jai-Youl Lee; Sang-Won Choi; Jong-Wook Park; Taeg Kyu Kwon
- Keimyung Author(s)
- Park, Jong Wook; Kwon, Taeg Kyu
- Department
- Dept. of Immunology (면역학)
- Journal Title
- European Journal of Pharmacology
- Issued Date
- 2004
- Volume
- 494
- Issue
- 1
- Abstract
- Triptolide (PG490) is a natural, biologically active compound extracted from the Chinese herb Tripterygium wilfordii. It has been shown to
possess potent anti-inflammatory and immunosuppressive properties. In Raw 264.7 cells stimulated with lipopolysaccharide (LPS) to mimic
inflammation, triptolide inhibits nitric oxide (NO) production in a dose-dependent manner and abrogates inducible nitric oxide synthase (iNOS)
gene expression. To investigate the mechanism by which triptolide inhibits murine iNOS gene expression, we examined activation of mitogenactivated
protein kinases (MAP kinases) and nuclear factor-nB (NF-nB) in these cells. Addition of triptolide inhibited phosphorylation of c-Jun
NH2-terminal kinase (JNK) but not that of extracellular signal-regulated kinase (ERK) or p38 mitogen-activated protein kinase. In addition,
triptolide significantly inhibited the DNA binding activity of NF-nB. Taken together, these results suggest that triptolide acts to inhibit
inflammation through inhibition of NO production and iNOS expression through blockade of NF-nB and JNK activation.
D 2004 Elsevier B.V. All rights reserved.
Keywords: Triptolide; NO (Nitric oxide); iNOS; NF-nB; JNK
- Authorize & License
-
- Authorize공개
- EmbargoForever
- Files in This Item:
-
Items in Repository are protected by copyright, with all rights reserved, unless otherwise indicated.