2. Academic Validation
  3. β-Caryophyllene Acts as a Ferroptosis Inhibitor to Ameliorate Experimental Colitis

β-Caryophyllene Acts as a Ferroptosis Inhibitor to Ameliorate Experimental Colitis

  • Int J Mol Sci. 2022 Dec 16;23(24):16055. doi: 10.3390/ijms232416055.
Yan-Ting Wu 1 2 3 4 5 6,  Li-Shan Zhong 1 2 3 4,  Chen Huang 1 2 3 4,  Yu-Ying Guo 1 4 5 6,  Fu-Jun Jin 1,  Yu-Ze Hu 1 2 3 4,  Zi-Bo Zhao 1 2 3 4,  Zhe Ren 1 2 3 4 5 6,  Yi-Fei Wang 1 2 3 4 5 6
Affiliations

Affiliations

  • 1 Department of Cell Biology, College of Life Science and Technology, Jinan University, Guangzhou 510632, China.
  • 2 Guangdong Province Key Laboratory of Bioengineering Medicine, Jinan University, Guangzhou 510632, China.
  • 3 Guangdong Provincial Biotechnology Drug & Engineering Technology Research Center, Jinan University, Guangzhou 510632, China.
  • 4 National Engineering Research Center for Modernization of Traditional Chinese Medicine Moxa Herb Branch, Guangzhou 510632, China.
  • 5 Key Laboratory of Innovative Technology Research on Natural Products and Cosmetics Raw Materials, Guangzhou 510632, China.
  • 6 National Engineering and Technology Research Center of Modernization of Traditional Chinese Medicine Artemisia Argyi Branch Center, Guangzhou 510632, China.
PMID: 36555694 DOI: 10.3390/ijms232416055
Abstract

Macrophage infiltration is one of the main pathological features of ulcerative colitis (UC) and Ferroptosis is a type of nonapoptotic cell death, connecting oxidative stress and inflammation. However, whether Ferroptosis occurs in the colon macrophages of UC mice and whether targeting macrophage Ferroptosis is an effective approach for UC treatment remain unclear. The present study revealed that macrophage lipid peroxidation was observed in the colon of UC mice. Subsequently, we screened several main components of essential oil from Artemisia argyi and found that β-caryophyllene (BCP) had a good inhibitory effect on macrophage lipid peroxidation. Additionally, ferroptotic macrophages were found to increase the mRNA expression of tumor necrosis factor alpha (Tnf-α) and prostaglandin-endoperoxide synthase 2 (Ptgs2), while BCP can reverse the effects of inflammation activated by Ferroptosis. Further molecular mechanism studies revealed that BCP activated the type 2 Cannabinoid Receptor (CB2R) to inhibit macrophage Ferroptosis and its induced inflammatory response both in vivo and in vitro. Taken together, BCP potentially ameliorated experimental colitis inflammation by inhibiting macrophage Ferroptosis. These results revealed that macrophage Ferroptosis is a potential therapeutic target for UC and identified a novel mechanism of BCP in ameliorating experimental colitis.

Keywords

ferroptosis; inflammation; macrophage; type 2 cannabinoid receptor; ulcerative colitis; β-caryophyllene.

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