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J Biomed Sci. 2013 Oct 31;20:84. doi: 10.1186/1423-0127-20-84.

Wedelolactone inhibits LPS-induced pro-inflammation via NF-kappaB pathway in RAW 264.7 cells.

Author information

1
Department of Pharmacy, the Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, China. gdpufredayuan@163.com.

Abstract

BACKGROUND:

Wedelolactone (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.

RESULTS:

To 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.

CONCLUSIONS:

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

PMID:
24176090
PMCID:
PMC4174895
DOI:
10.1186/1423-0127-20-84
[Indexed for MEDLINE]
Free PMC Article

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