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      5, 7, 2′, 4′, 5′-Pentamethoxyflavanone regulates M1/M2 macrophage phenotype and protects the septic mice

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          Abstract

          Flavonoids have been reported to exert protective effect against many inflammatory diseases, while the underlying cellular mechanisms are still not completely known. In the present study, we explored the anti-inflammation activity of 5, 7, 2′, 4′, 5′-pentamethoxyflavanone (abbreviated as Pen.), a kind of polymethoxylated flavonoid, both in vitro and in vivo experiments. Pen. was showed no obvious toxicity in macrophages even at high dosage treatment. Our results indicated that Pen. significantly inhibited both mRNA and protein level of proinflammatory cytokines, IL-1β, IL-6, TNF-α and iNOS, which was characteristic expressed on M1 polarized macrophages. These effects of Pen. were further confirmed by diminished expression of CD11c, the M1 macrophage surface marker. Further researches showed that the mechanism was due to that Pen. downregulated the activity of p65, key transcription factor for M1 polarization. On the other hand, Pen. also enhanced M2 polarization with upregulation of anti-inflammatory factors and increase of M2 macrophage surface markers, which lead to the balance of M1 and M2 macrophages. Moreover, in vivo research verified that Pen. treatment alleviated LPS-induced sepsis in mice by increasing survival rate, decreasing inflammatory cytokines and improving lung tissue damage. In summary, our results suggested that Pen. modulated macrophage phenotype via suppressing p65 signal pathway to exert the anti-inflammation activity.

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          Author and article information

          Journal
          CJNM
          Chinese Journal of Natural Medicines
          Elsevier
          1875-5364
          20 May 2019
          : 17
          : 5
          : 363-371
          Affiliations
          1 State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210023, China
          Author notes
          *Corresponding authors: WU Xu-Dong, Tel: 86-25-89687620, E-mail: xudongwu@ 123456nju.edu.cn ; XU Qiang, Email: molpharm@ 123456163.com

          These authors have no conflict of interest to declare.

          Article
          S1875-5364(19)30042-1
          10.1016/S1875-5364(19)30042-1
          31171271
          Copyright © 2019 China Pharmaceutical University. Published by Elsevier B.V. All rights reserved.
          Funding
          Funded by: National Natural Science Foundation of China
          Award ID: 81872916
          Award ID: 81673487
          Award ID: 81473221
          Funded by: The Drug Innovation Major Project" of National Science Technology Ministry
          Award ID: 2018ZX09711001-003-007
          Funded by: Natural Science Foundation of Jiangsu Province
          Award ID: BK20161399
          Funded by: Fundamental Research Funds for the Central Universities
          Award ID: 020814380118
          This work was supported by the National Natural Science Foundation of China (Nos. 81872916, 81673487, and 81473221), "The Drug Innovation Major Project" of National Science Technology Ministry (No. 2018ZX09711001-003-007), the Natural Science Foundation of Jiangsu Province (No. BK20161399), and the Fundamental Research Funds for the Central Universities (No. 020814380118).

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