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Title 

Triptolide inhibits murine-inducible nitric oxide synthase expression by down-regulating lipopolysaccharide-induced activity of nuclear factor-κB and c-Jun NH2-terminal kinase

Authors 

Y H KimSang-Han LeeJ Y LeeS W ChoiJ W ParkT K Kwon

Publisher 

Elsevier

Issue Date 

2004

Citation 

European Journal of Pharmacology, vol. 494, no. 1, pp. 1-9

Keywords 

iNOSJNKNF-κBNO (Nitric oxide)triptolide2 morpholino 8 phenylchromoneanthra[1,9 cd]pyrazol 6(2h) oneimmunoglobulin enhancer binding proteininducible nitric oxide synthaselipopolysaccharide

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 mitogen-activated protein kinases (MAP kinases) and nuclear factor-κB (NF-κB) 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-κB. Taken together, these results suggest that triptolide acts to inhibit inflammation through inhibition of NO production and iNOS expression through blockade of NF-κB and JNK activation.

ISSN 

0014-2999

Link 

http://dx.doi.org/10.1016/j.ejphar.2004.04.040

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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