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Food Chem Toxicol. 2013 Aug;58:479-86. doi: 10.1016/j.fct.2013.05.031. Epub 2013 May 28.

Suppression of iNOS and COX-2 expression by flavokawain A via blockade of NF-κB and AP-1 activation in RAW 264.7 macrophages.

Author information

1
Department of Biomedical Science, Hallym University, Chunchon, Republic of Korea.

Abstract

Flavokawain A, a major constituent of chalcones derived from kava extracts, exerts various biological activities such as anti-tumor activities. In this study, we examined the suppressive effect of flavokawain A on LPS-induced expression of pro-inflammatory mediators and the molecular mechanisms responsible for these activities in the murine macrophages. Flavokawain A significantly suppressed expression of iNOS and COX-2, as well as the subsequent production of NO and PGE2 in the LPS-stimulated RAW 264.7 cells. Flavokawain A significantly inhibited LPS-induced activation of NF-κB and AP-1 signaling pathways. In addition, flavokawain A inhibited activation of JNK and p38 MAPK which was responsible for expression of iNOS and COX-2 in the LPS-stimulated RAW 264.7 cells. Furthermore, flavokawain A suppressed LPS-induced expression of pro-inflammatory cytokines, such as TNF-α, IL-1β and IL-6. These results suggest that flavokawain A may exert anti-inflammatory responses by suppressing LPS-induced expression of pro-inflammatory mediators via blockage of NF-κB-AP-1-JNK/p38 MAPK signaling pathways in the murine macrophages.

KEYWORDS:

3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide; AP-1; COX-2; DMEM; Dulbecco’s modified eagle medium; ELISA; FBS; Flavokawain A; HRP; Inflammation; IκBα; LPS; MTT; Macrophages; NF-κB; NO; PCR; PGE(2); SDS; TLR4; activator protein-1; cyclooxygenase; enzyme linked immune sorbent assay; fetal bovine serum; horseradish peroxidase; iNOS; inducible NO synthase; inhibitor of kappa B alpha; lipopolysaccharides; nitric oxide; nuclear factor-κB; polymerase chain reaction; prostaglandin E(2); sodium dodecyl sulphate; toll-like receptor 4

PMID:
23727179
DOI:
10.1016/j.fct.2013.05.031
[Indexed for MEDLINE]

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