AIMS OF STUDY: Although the flowers of Chrysanthemum indicum Linné (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-1beta by ELISA, mRNA and protein expression of iNOS and COX-2, phosphorylation of MAPKs, and activation of NF-kappaB 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-1beta 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-kappaB p65 subunits, which correlated with an inhibitory effect on IkappaBalpha 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-1beta, via suppression of MAPKs and NF-kappaB-dependent pathways.
AIMS OF STUDY: Although the flowers of Chrysanthemum indicum Linné (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-1beta by ELISA, mRNA and protein expression of iNOS and COX-2, phosphorylation of MAPKs, and activation of NF-kappaB 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-1beta 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-kappaB p65 subunits, which correlated with an inhibitory effect on IkappaBalpha 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-1beta, via suppression of MAPKs and NF-kappaB-dependent pathways.
Authors: Mouna Achoui; David Appleton; Mahmood Ameen Abdulla; Khalijah Awang; Mustafa Ali Mohd; Mohd Rais Mustafa Journal: PLoS One Date: 2010-12-01 Impact factor: 3.240
Authors: M A Sunil; V S Sunitha; Prasanthkumar Santhakumaran; Mohind C Mohan; Midhun Sebastian Jose; E K Radhakrishnan; Jyothis Mathew Journal: Inflammopharmacology Date: 2021-06-11 Impact factor: 4.473
Authors: Mao-Qiang Man; Melanie Hupe; Richard Sun; George Man; Theodora M Mauro; Peter M Elias Journal: Evid Based Complement Alternat Med Date: 2012-11-19 Impact factor: 2.629