期刊论文详细信息
BMC Complementary and Alternative Medicine
An ethyl acetate fraction derived from Houttuynia cordata extract inhibits the production of inflammatory markers by suppressing NF-кB and MAPK activation in lipopolysaccharide-stimulated RAW 264.7 macrophages
Ho Kyoung Kim1  Byeong Cheol Moon1  A Yeong Lee1  Hyo Seon Kim1  Kyoung Jin Nho1  Jin Mi Chun1 
[1] Herbal Medicine Resources Group, Korea Institute of Oriental Medicine, Yuseongdae-ro 1672, Yuseong-gu, Daejeon 305-811, Republic of Korea
关键词: Mitogen-activated protein kinase;    Nuclear factor-κB;    Cyclooxygenase-2;    Inducible nitric oxide synthase;    Houttuynia cordata;   
Others  :  1087401
DOI  :  10.1186/1472-6882-14-234
 received in 2013-08-16, accepted in 2014-06-30,  发布年份 2014
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【 摘 要 】

Background

Houttuynia cordata Thunb. (Saururaceae) has been used in traditional medicine for treatment of inflammatory diseases. This study evaluated the anti-inflammatory effects of an ethyl acetate fraction derived from a Houttuynia cordata extract (HCE-EA) on the production of inflammatory mediators and the activation of nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPKs) in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages.

Methods

To measure the effects of HCE-EA on pro-inflammatory cytokine and inflammatory mediator’s expression in RAW 264.7 cells, we used the following methods: cell viability assay, Griess reagent assay, enzyme-linked immunosorbent assay, real-time polymerase chain reaction and western blotting analysis.

Results

HCE-EA downregulated nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), and interleukin (IL-6) production in the cells, as well as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression. Furthermore, HCE-EA suppressed nuclear translocation of the NF-κB p65 subunit, which correlated with an inhibitory effect on IκBα (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha) phosphorylation. HCE-EA also attenuated the activation of MAPKs (p38 and JNK).

Conclusions

Our results suggest that the anti-inflammatory properties of HCE-EA may stem from the inhibition of pro-inflammatory mediators via suppression of NF-κB and MAPK signaling pathways.

【 授权许可】

   
2014 Chun et al.; licensee BioMed Central Ltd.

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