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β-Caryophyllene Acts as a Ferroptosis Inhibitor to Ameliorate Experimental Colitis
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 fer...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9784863/ https://www.ncbi.nlm.nih.gov/pubmed/36555694 http://dx.doi.org/10.3390/ijms232416055 |
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author | Wu, Yan-Ting Zhong, Li-Shan Huang, Chen Guo, Yu-Ying Jin, Fu-Jun Hu, Yu-Ze Zhao, Zi-Bo Ren, Zhe Wang, Yi-Fei |
author_facet | Wu, Yan-Ting Zhong, Li-Shan Huang, Chen Guo, Yu-Ying Jin, Fu-Jun Hu, Yu-Ze Zhao, Zi-Bo Ren, Zhe Wang, Yi-Fei |
author_sort | Wu, Yan-Ting |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-9784863 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-97848632022-12-24 β-Caryophyllene Acts as a Ferroptosis Inhibitor to Ameliorate Experimental Colitis Wu, Yan-Ting Zhong, Li-Shan Huang, Chen Guo, Yu-Ying Jin, Fu-Jun Hu, Yu-Ze Zhao, Zi-Bo Ren, Zhe Wang, Yi-Fei Int J Mol Sci Article 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. MDPI 2022-12-16 /pmc/articles/PMC9784863/ /pubmed/36555694 http://dx.doi.org/10.3390/ijms232416055 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Wu, Yan-Ting Zhong, Li-Shan Huang, Chen Guo, Yu-Ying Jin, Fu-Jun Hu, Yu-Ze Zhao, Zi-Bo Ren, Zhe Wang, Yi-Fei β-Caryophyllene Acts as a Ferroptosis Inhibitor to Ameliorate Experimental Colitis |
title | β-Caryophyllene Acts as a Ferroptosis Inhibitor to Ameliorate Experimental Colitis |
title_full | β-Caryophyllene Acts as a Ferroptosis Inhibitor to Ameliorate Experimental Colitis |
title_fullStr | β-Caryophyllene Acts as a Ferroptosis Inhibitor to Ameliorate Experimental Colitis |
title_full_unstemmed | β-Caryophyllene Acts as a Ferroptosis Inhibitor to Ameliorate Experimental Colitis |
title_short | β-Caryophyllene Acts as a Ferroptosis Inhibitor to Ameliorate Experimental Colitis |
title_sort | β-caryophyllene acts as a ferroptosis inhibitor to ameliorate experimental colitis |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9784863/ https://www.ncbi.nlm.nih.gov/pubmed/36555694 http://dx.doi.org/10.3390/ijms232416055 |
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