Chen Chin-Chaun, Lin Ming-Wei, Liang Chan-Jung, Wang Shu-Huei
Graduate Institute of Natural Products, Chang Gung University, Taoyuan, Taiwan.
Chinese Herbal Medicine Research Team, Healthy Aging Research Center, Chang Gung University, Taoyuan, Taiwan.
PLoS One. 2016 Jul 14;11(7):e0158662. doi: 10.1371/journal.pone.0158662. eCollection 2016.
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.
泽兰黄素是从朝鲜艾(菊科)中分离出的一种黄酮。本研究的目的是检测泽兰黄素在脂多糖(LPS)处理的RAW264.7巨噬细胞以及LPS诱导的小鼠皮肤和肺部炎症模型中的抗炎作用,并确定其作用机制。泽兰黄素减少了LPS诱导的RAW264.7巨噬细胞中炎性介质(诱导型一氧化氮合酶、环氧化酶-2和一氧化氮)和促炎细胞因子(白细胞介素-6和肿瘤坏死因子-α)的释放。泽兰黄素抑制了LPS诱导的p38丝裂原活化蛋白激酶、细胞外信号调节激酶1/2、c-Jun氨基末端激酶、蛋白激酶B和p65的磷酸化以及p65和c-fos的核转位。这些作用主要是通过抑制c-Jun氨基末端激酶介导的。在小鼠爪部和肺部模型中,泽兰黄素有效抑制了LPS诱导的水肿形成,并下调了诱导型一氧化氮合酶和环氧化酶-2的表达。这些结果表明泽兰黄素具有抗炎特性,并提示泽兰黄素可开发成为一种抗炎剂。