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Siegesbeckia pubescens Makino inhibits Pam3CSK4-induced inflammation in RAW 264.7 macrophages through suppressing TLR1/TLR2-mediated NF-ΚB activation
Sang W.1; Zhong Z.1,4; Linghu K.1; Xiong W.1; Tse A.K.W.5; Cheang W.S.1; Yu H.1,2,3,6; Wang Y.1,7
2018
Source PublicationChinese Medicine (United Kingdom)
Volume13Issue:1
Abstract

Background: Siegesbeckia pubescens Makino (SP) is one of the important plant origins for the anti-inflammatory Chinese herbal medicine of Siegesbeckiae Herba. The current investigations indicated that the anti-inflammatory effects of SP were associated with the toll-like receptors (TLRs)-mediated nuclear factor-ΚB (NF-ΚB) and the mitogen-activated protein kinase (MAPK) signaling pathways. Methods: Raw 264.7 macrophages were pretreated with the 50% ethanol extract of SP (SPE, 50-200 μg/mL) and then co-treated with Pam3CSK4 (200 ng/mL) for another 12 h. The inhibitory effect of SPE on Pam3CSK4-stimulated NO release and post-inflammatory cytokines secretions were determined using Griess reagent and Elisa kits, respectively. The influence of SPE on NF-ΚB and MAPKs signaling relevant proteins was measured by Western blotting analysis, while the intracellular nitric oxide (NO) generation and NF-ΚB/p65 nuclear translocation were determined using Leica TCS SP8 laser scanning confocal microscope. Moreover, the effect of SPE on luciferase reporter gene in NF-ΚB-luc DNA transfected raw 264.7 cells was determined using the Dual-Glo luciferase assay system kit. Results: SPE dose-dependently (50-200 μg/mL) attenuated Pam3CSK4-induced NO release, post-inflammatory cytokines (IL-6, TNF-α and MCP-1) secretions and intracellular NO generation in raw 264.7 cells. Biologically, SPE suppressed Pam3CSK4-induced expressions of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), phosphorylation of NF-ΚB/p65 and IΚBα, but did not significantly show effect on the proteins involved in MAPKs signaling (p38, ERK and JNK). The results were further confirmed by NF-ΚB-luc reporter gene assay and p65 nuclear translocation assay. Conclusions: In conclusion, SPE ameliorated Pam3CSK4-induced inflammation in raw 264.7 cells through suppressing TLR 1/2-mediated NF-ΚB activation. © 2018 The Author(s).

KeywordInflammation Nf-κb Pam3csk4 Siegesbeckia Pubescens Makino Toll-like Receptor 1/2
DOI10.1186/s13020-018-0193-x
URLView the original
Language英語English
The Source to ArticleScopus
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Cited Times [WOS]:18   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionInstitute of Chinese Medical Sciences
Affiliation1.University of Macau, Institute of Chinese Medical Sciences, State Key Laboratory of Quality Research in Chinese Medicine, Macao, China
2.HKBU Shenzhen Research Center, Shenzhen, Guangdong, China
3.Hong Kong Baptist University, School of Chinese Medicine, Kowloon Tong, Hong Kong, China
4.Guangdong Medical University, Guangdong Key Laboratory for Research and Development of Natural Drugs, Zhanjiang, China
5.Southern University of Science and Technology, Academy for Advanced Interdisciplinary Studies, Shenzhen, Guangdong, China
6.University of Macau, Institute of Chinese Medical Sciences, Building N22, Avenida da Universidade, Taipa, Macao SAR, China
7.University of Macau, Institute of Chinese Medical Sciences, Building N22, Avenida da Universidade, Taipa, Macao SAR, China
First Author AffilicationInstitute of Chinese Medical Sciences
Recommended Citation
GB/T 7714
Sang W.,Zhong Z.,Linghu K.,et al. Siegesbeckia pubescens Makino inhibits Pam3CSK4-induced inflammation in RAW 264.7 macrophages through suppressing TLR1/TLR2-mediated NF-ΚB activation[J]. Chinese Medicine (United Kingdom),2018,13(1).
APA Sang W.,Zhong Z.,Linghu K.,Xiong W.,Tse A.K.W.,Cheang W.S.,Yu H.,&Wang Y..(2018).Siegesbeckia pubescens Makino inhibits Pam3CSK4-induced inflammation in RAW 264.7 macrophages through suppressing TLR1/TLR2-mediated NF-ΚB activation.Chinese Medicine (United Kingdom),13(1).
MLA Sang W.,et al."Siegesbeckia pubescens Makino inhibits Pam3CSK4-induced inflammation in RAW 264.7 macrophages through suppressing TLR1/TLR2-mediated NF-ΚB activation".Chinese Medicine (United Kingdom) 13.1(2018).
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