Gambogenic acid inhibits LPS-simulated inflammatory response by suppressing NF-B and MAPK in macrophages

Xianjun Yu, Qun Zhao, Haiwei Zhang, Cunxian Fan, Xixi Zhang, Qun Xie, Chengxian Xu, Yongbo Liu, Xiaoxia Wu, Simon Q B HAN, Haibing Zhang*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

9 Citations (Scopus)

Abstract

Inflammation is a response of body tissues to injury and infection. Compounds that can inhibit inflammation have been shown to have potential therapeutic clinical application. Gambogenic acid (GEA) has potent antitumor and anti-inflammatory activities. Herein, the molecular mechanisms of GEA's anti-inflammatory effect were investigated in lipopolysaccharide (LPS)-stimulated macrophage cells. The results showed that pretreatment with GEA could markedly inhibit interleukin (IL)-1α, IL-1β, tumor necrosis factor-α, IFN-β, IL-12b, and IL-23a production in a dose-dependent manner in LPS-induced model. Furthermore, this drug significantly reduced the release of nitric oxide (NO), and impaired the protein level of inducible NO synthase and the cyclooxygenase 2. The finding also showed that the effect of GEA may be related to the suppression of the nuclear factor-B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathway. These results indicate that GEA could suppress LPS-simulated inflammatory response partially by attenuating NO synthesis and NF-κB and MAPK activation, suggesting that it may become a potent therapeutic agent for the treatment of inflammatory diseases.

Original languageEnglish
Pages (from-to)454-461
Number of pages8
JournalActa Biochimica et Biophysica Sinica
Volume48
Issue number5
DOIs
Publication statusPublished - 1 May 2016

Scopus Subject Areas

  • Biophysics
  • Biochemistry

User-Defined Keywords

  • B pathway
  • gambogenic acid
  • inflammation
  • MAPK pathway
  • NF-κ
  • NO

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