Xiao Qing Long Tang essential oil exhibits inhibitory effects on the release of pro-inflammatory mediators by suppressing NF-κB, AP-1, and IRF3 signalling in the lipopolysaccharide-stimulated RAW264.7 cells
Autor: | Hui Zhao, Gan Luo, Li-Shan Yan, Si-Yuan Pan, Yu Ding, Xiu-Qiong Fu, Shuo-Feng Zhang, Yi Zhang, Jing Kong, Yan-Ling Liu, Brian Chi-Yan Cheng |
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Rok vydání: | 2019 |
Předmět: |
Chemokine
Lipopolysaccharide biology Chemistry Kinase General Chemical Engineering NF-κB 02 engineering and technology General Chemistry 010402 general chemistry 021001 nanoscience & nanotechnology 01 natural sciences Molecular biology 0104 chemical sciences chemistry.chemical_compound biology.protein Phosphorylation Secretion Viability assay 0210 nano-technology Protein kinase B |
Zdroj: | RSC Advances. 9:12977-12989 |
ISSN: | 2046-2069 |
Popis: | Xiao Qing Long Tang (literally “Minor blue dragon decoction” in Chinese), a traditional Chinese formula, is prescribed to treat respiratory diseases. However, only few studies have been reported on its anti-inflammatory mechanisms. In this study, we investigated the inhibitory effects of Xiao Qing Long Tang essential oil on inflammatory mediators and explored the mechanisms of action of XQEO in the lipopolysaccharide (LPS)-stimulated RAW264.7 cells. XQEO was prepared via steam distillation and characterized by GC-MS analysis. MTT and Griess assays were used to measure cell viability and NO production, respectively. The mRNA expression and the production of LPS-induced pro-inflammatory cytokines (IL-1β, IL-6, TNF-α, and IL-10) and chemokines (MCP-1, Rantes, and MIP-1α) were determined by real-time PCR and enzyme-linked immunosorbent assay, respectively. Furthermore, we determined the protein levels of the components of NF-κB, AP-1 and IRF3 signalling by Western blotting. Immunofluorescence assay was used to estimate the nuclear translocation of NF-κB, AP-1 and IRF3. The results showed that XQEO inhibited the secretion of NO and PGE2 and down-regulated the mRNA and protein levels of iNOS and COX-2. We also found that XQEO suppressed the LPS-induced overproduction of pro-inflammatory mediators. Moreover, XQEO inhibited the phosphorylation of NF-κB/p65, AP-1/c-Jun, and IRF3 by suppressing their upstream kinases, such as MAPKs, TBK1, Akt, IKKα/β, and IκB, reducing the LPS-induced NF-κB, AP-1 and IRF3 translocation to the nucleus. These findings suggest that XQEO effectively suppresses the production of pro-inflammatory mediators possibly through the inhibition of NF-κB, AP-1, and IRF3 signalling in the LPS-stimulated RAW264.7 cells. |
Databáze: | OpenAIRE |
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