Hericenone C attenuates the second phase of formalin-induced nociceptive behavior by suppressing the accumulation of CD11c-positive cells in the paw epidermis via phosphorylated P65

Junhao Li, Kengo Hamamura, Yuya Yoshida, Shimpei Kawano, Shohei Uchinomiya, Jiahongyi Xie, Damiana Scuteri, Kohei Fukuoka, Orion Zaitsu, Fumiaki Tsurusaki, Yuma Terada, Ryotaro Tsukamoto, Takumi Nishi, Taiki Fukuda, Kosuke Oyama, Giacinto Bagetta, Akio Ojida, Kuniyoshi Shimizu, Shigehiro Ohdo, Naoya Matsunaga

Research output: Contribution to journalArticlepeer-review

Abstract

Hericenone C is one of the most abundant secondary metabolites derived from Hericium erinaceus, under investigation for medicinal properties. Here, we report that Hericenone C inhibits the second phase of formalin-induced nociceptive behavior in mice. As the second phase is involved in inflammation, in a mechanistic analysis on cultured cells targeting NF-κB response element (NRE): luciferase (Luc)-expressing cells, lipopolysaccharide (LPS)-induced NRE::Luc luciferase activity was found to be significantly inhibited by Hericenone C. Phosphorylation of p65, which is involved in the inflammatory responses of the NF-κB signaling pathway, was also induced by LPS and significantly reduced by Hericenone C. Additionally, in mice, the number of CD11c-positive cells increased in the paw during the peak of the second phase of the formalin test, which decreased upon Hericenone C intake. Our findings confirm the possibility of Hericenone C as a novel therapeutic target for pain-associated inflammation.

Original languageEnglish
Article number150077
JournalBiochemical and Biophysical Research Communications
Volume720
DOIs
Publication statusPublished - Aug 6 2024

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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