Chtysanthemum indicum Linne extract inhibits the inflammatory response by suppressing NF-κB and MAPKs activation in lipopolysaccharide-induced RAW 264.7 macrophages

被引:75
|
作者
Cheon, Myeong Sook [1 ]
Yoon, Taesook [1 ]
Lee, Do Yeon [1 ]
Choi, Goya [1 ]
Moon, Byeong Cheol [1 ]
Lee, A-Yeong [1 ]
Choo, Byung Kil [1 ]
Kim, Ho Kyoung [1 ]
机构
[1] Korea Inst Oriental Med, Dept Herbal Resources Res, Taejon 305811, South Korea
关键词
Anti-inflammation; Asteraceae; Chrysanthemum indicum; COX-2; iNOS; Macrophages; MAPKs; NF-kappa B; NITRIC-OXIDE SYNTHASE; MEDICINAL FLOWERS; ABSOLUTE STEREOSTRUCTURES; RAW-264.7; MACROPHAGES; SIGNAL-TRANSDUCTION; ALDOSE REDUCTASE; PROTEIN-KINASE; EXPRESSION; INDUCTION; CANCER;
D O I
10.1016/j.jep.2009.01.034
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Aims of study: Although the flowers of Chrysanthemurn indicum Linne (Asteraceae) have long been used in traditional Korean and Chinese medicine to treat inflammatory diseases, the underlying mechanism(s) by which these effects are induced remains to be defined. We investigated the effects of a 70% ethanolic extract of C. indicum (CIE) on the activities of cellular signaling molecules that mediate inflammatory responses. Materials and methods: Production of NO, PGE(2), TNF-alpha, and IL-1 beta by ELISA, mRNA and protein expression of iNOS and COX-2, phosphorylation of MAPKs, and activation of NF-kappa B by RT-PCR and Western blotting were examined in LPS-induced RAW 264.7 macrophages. Results: The CIE strongly inhibited NO, PGE(2), TNF-alpha, and IL-1 beta production, and also significantly inhibited mRNA and protein expression of iNOS and COX-2 in LPS-induced RAW 264.7 macrophages, in a dose-dependent manner. Furthermore, the CIE clearly suppressed nuclear translocation of NF-kappa B p65 subunits, which correlated with an inhibitory effect on I kappa B alpha phosphorylation. The CIE also attenuated the activation of ERK1/2 and JNK in a dose-dependent manner. Conclusion: Our results suggest that the anti-inflammatory properties of CIE might result from the inhibition of inflammatory mediators, such as NO, PGE(2), TNF-alpha, and IL-1 beta, via suppression of MAPKs and NF-kappa B-depenclent pathways. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:473 / 477
页数:5
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