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

BMC Complementary and Alternative Medicine

Research Article

Byeong Cheol Moon¹  Jin Mi Chun¹  Kyoung Jin Nho¹  Ho Kyoung Kim¹  Hyo Seon Kim¹  A Yeong Lee¹ 

[1] Herbal Medicine Resources Group, Korea Institute of Oriental Medicine, Yuseongdae-ro 1672, 305-811, Yuseong-gu, Daejeon, Republic of Korea;

关键词: Houttuynia cordata;    Inducible nitric oxide synthase;    Cyclooxygenase-2;    Nuclear factor-κB;    Mitogen-activated protein kinase;   

DOI  :  10.1186/1472-6882-14-234

 received in 2013-08-16, accepted in 2014-06-30,  发布年份 2014

来源: Springer

【 摘 要 】

BackgroundHouttuynia 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.MethodsTo 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.ResultsHCE-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).ConclusionsOur 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】

Unknown   
© Chun et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited.