The Anti-Inflammatory Effects and Mechanisms of Eupafolin in Lipopolysaccharide-Induced Inflammatory Responses in RAW264.7 Macrophages.

Abstract

Eupafolin is a flavone isolated from Artemisia princeps Pampanini (family Asteraceae). The aim of this study was to examine the anti-inflammatory effects of eupafolin in lipopolysaccharide (LPS)-treated RAW264.7 macrophages and LPS-induced mouse skin and lung inflammation models and to identify the mechanism underlying these effects. Eupafolin decreased the LPS-induced release of inflammatory mediators (iNOS, COX-2 and NO) and proinflammatory cytokines (IL-6 and TNF-α) from the RAW264.7 macrophages. Eupafolin inhibited the LPS-induced phosphorylation of p38 MAPK, ERK1/2, JNK, AKT and p65 and the nuclear translocation of p65 and c-fos. These effects were mainly mediated by the inhibition of JNK. In the mouse paw and lung models, eupafolin effectively suppressed the LPS-induced edema formation and down-regulated iNOS and COX-2 expression. These results demonstrated that eupafolin exhibits anti-inflammatory properties and suggested that eupafolin can be developed as an anti-inflammatory agent.

• Authors: Chin-Chaun Chen, Ming-Wei Lin, Chan-Jung Liang, Shu-Huei Wang
• Journal: PloS one (PLoS One) Vol. 11 Issue 7 Pg. e0158662 ( 2016) ISSN: 1932-6203 [Electronic] United States
• PMID: 27414646 (Publication Type: Journal Article)

Chemical References

• Anti-Inflammatory Agents
• Flavones
• Interleukin-6
• Lipopolysaccharides
• Tumor Necrosis Factor-alpha
• Nitric Oxide
• Nitric Oxide Synthase Type II
• Cyclooxygenase 2
• eupafolin

Topics

• Animals
• Anti-Inflammatory Agents (pharmacology)
• Cyclooxygenase 2 (metabolism)
• Flavones (pharmacology)
• Inflammation (chemically induced, metabolism)
• Interleukin-6 (metabolism)
• Lipopolysaccharides
• Lung (drug effects, metabolism)
• Macrophages (drug effects, metabolism)
• Mice
• Nitric Oxide (metabolism)
• Nitric Oxide Synthase Type II (metabolism)
• Phosphorylation
• Signal Transduction (drug effects)
• Skin (drug effects, metabolism)
• Tumor Necrosis Factor-alpha (metabolism)