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

• Published in: BMC complementary and alternative medicine 2014-07, Vol.14 (1), p.234-234, Article 234
• Main Authors: Chun, Jin Mi, Nho, Kyoung Jin, Kim, Hyo Seon, Lee, A Yeong, Moon, Byeong Cheol, Kim, Ho Kyoung
• Format: Article
• Language: English
• Subjects: Acetates - chemistry; Animals; Anti-Inflammatory Agents - chemistry; Anti-Inflammatory Agents - pharmacology; Cell Line, Tumor; cell viability; complement; Cyclooxygenase 2 - metabolism; Drugs, Chinese Herbal - chemistry; Drugs, Chinese Herbal - pharmacology; enzyme-linked immunosorbent assay; ethyl acetate; genes; Houttuynia cordata; inducible nitric oxide synthase; interleukin-6; lipopolysaccharides; Lipopolysaccharides - pharmacology; macrophages; Macrophages - drug effects; Macrophages - enzymology; Macrophages - metabolism; MAP Kinase Signaling System - drug effects; Mice; mitogen-activated protein kinase; Mitogen-Activated Protein Kinases - metabolism; necrosis; neoplasms; NF-kappa B - metabolism; nitric oxide; Nitric Oxide - metabolism; Nitric Oxide Synthase Type II - metabolism; phosphorylation; polypeptides; prostaglandin synthase; prostaglandins; quantitative polymerase chain reaction; Saururaceae; traditional medicine; viability assays
• ISSN: 1472-6882; 1472-6882
• DOI: 10.1186/1472-6882-14-234

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. 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. 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). 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.