1. Academic Validation
  2. 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

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

  • Biochem Biophys Res Commun. 2024 Aug 6:720:150077. doi: 10.1016/j.bbrc.2024.150077.
Junhao Li 1 Kengo Hamamura 1 Yuya Yoshida 1 Shimpei Kawano 1 Shohei Uchinomiya 2 Jiahongyi Xie 3 Damiana Scuteri 4 Kohei Fukuoka 1 Orion Zaitsu 1 Fumiaki Tsurusaki 1 Yuma Terada 1 Ryotaro Tsukamoto 1 Takumi Nishi 1 Taiki Fukuda 1 Kosuke Oyama 5 Giacinto Bagetta 6 Akio Ojida 2 Kuniyoshi Shimizu 3 Shigehiro Ohdo 1 Naoya Matsunaga 7
Affiliations

Affiliations

  • 1 Department of Clinical Pharmacokinetics, Faculty of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi Higashi-ku, Fukuoka, 812-8582, Japan.
  • 2 Department of Medical Chemistry and Chemical Biology, Faculty of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi Higashi-ku, Fukuoka, 812-8582, Japan.
  • 3 Department of Agro-Environmental Sciences, Graduate School of Bioresources and Bioenvironmental Sciences, Kyushu University, Fukuoka, 819-0395, Japan.
  • 4 Department of Health Sciences, Magna Graecia University of Catanzaro, Catanzaro, 88100, Italy.
  • 5 Department of Clinical Pharmacokinetics, Faculty of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi Higashi-ku, Fukuoka, 812-8582, Japan; Department of Biological Science and Technology, Tokyo University of Science, Niijuku, Katsushika-ku, Tokyo, 125-8585, Japan.
  • 6 Pharmacotechnology Documentation and Transfer Unit, Preclinical and Translational Pharmacology, Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, 87036, Italy.
  • 7 Department of Clinical Pharmacokinetics, Faculty of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi Higashi-ku, Fukuoka, 812-8582, Japan. Electronic address: matunaga@phar.kyushu-u.ac.jp.
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.

Keywords

CD11c; Formalin test; Hericenone C; NF-κB; Nociceptive behavior; p65.

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