Wedelolactone inhibits LPS-induced pro-inflammation via NF-kappaB Pathway in RAW 264.7 cellsReportar como inadecuado

Wedelolactone inhibits LPS-induced pro-inflammation via NF-kappaB Pathway in RAW 264.7 cells - Descarga este documento en PDF. Documentación en PDF para descargar gratis. Disponible también para leer online.

Journal of Biomedical Science

, 20:84

First Online: 31 October 2013Received: 09 May 2013Accepted: 23 October 2013DOI: 10.1186-1423-0127-20-84

Cite this article as: Yuan, F., Chen, J., Sun, P. et al. J Biomed Sci 2013 20: 84. doi:10.1186-1423-0127-20-84


BackgroundWedelolactone WEL, a major coumestan ingredient in Wedelia chinensis, has been used to treat septic shock, hepatitis and venom poisoning in traditional Chinese medicines. The objective of the study was to elucidate the anti-inflammatory effects and mechanism of WEL with a cellular model of lipopolysaccharide LPS-induced RAW 264.7 cells.

ResultsTo study the role of WEL in pro-inflammation, we measured key inflammation mediators and end products including nitric oxide NO, prostaglandin E2 PGE2, inducible nitric oxide synthase iNOS, cyclooxygenase-2 COX-2 and tumor necrosis factor-α TNF-α by using the Griess method, enzyme linked immunosorbent assay ELISA and Western blotting. Nuclear factor-kappaB NF-κB transcription activity was detected by luciferase reporter assay. The important pro-inflammatory transcription factors, NF-κB p65 and inhibitory kappaB alpha IκB-α; and mitogen-activated protein kinases MAPKs, including extracellular signal-regulated kinase ERK, c-Jun N-terminal kinase JNK and p38 MAPK p38 were analyzed by Western blotting. Our study showed that WEL 0.1, 1, 10 μM significantly inhibited the protein expression levels of iNOS and COX-2 in LPS-stimulated cells, as well as the downstream products, including NO, PGE2 and TNF-α. Moreover, WEL also inhibited LPS-induced NF-κB p65 activation via the degradation and phosphorylation of IκB-α and subsequent translocation of the NF-κB p65 subunit to the nucleus.

ConclusionsOur results revealed that WEL has a potential to be a novel anti-inflammatory agent targeting on the NF-κB signaling pathway.

KeywordsWedelolactone WEL Popolysaccharide LPS Inflammation Nuclear factor-κB NF-κB Macrophage AbbreviationsWELWedelolactone



NONitric oxide

PGE2Prostaglandin E2

L-NAMEN-nitro-L-arginine methyl ester and lipopolysaccharide

iNOSInducible nitric oxide synthase


TNF-αTumor necrosis factor-α

ELISAEnzyme linked immunosorbent assay

NF-κBNuclear factor-kappaB

IκB-αInhibitory kappaB alpha

MAPKsMitogen-activated protein kinases

ERKExtracellular signal-regulated kinase

JNKc-Jun: N-terminal kinase

p-ERK1-2 and p-JNKPhosphorylation of ERK1-2 and JNK

T-ERK1-2t-JNK and t-p38, total ERK1-2, JNK and p38.

Electronic supplementary materialThe online version of this article doi:10.1186-1423-0127-20-84 contains supplementary material, which is available to authorized users.

Fang Yuan, Jie Chen contributed equally to this work.

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Autor: Fang Yuan - Jie Chen - Ping-ping Sun - Su Guan - Jing Xu


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