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Carvacrol protects mice against LPS-induced sepsis and attenuates inflammatory response in macrophages by modulating the ERK1/2 pathway

Macrophages play an important role in the development of life-threatening sepsis, which is characterized by multiorgan dysfunction, through their ability to produce inflammatory cytokines. Carvacrol is a phenolic compound that has been confirmed to possess strong anti‑inflammatory activity. In this...

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Autores principales: Yan, Chenghua, Kuang, Wendong, Jin, Liang, Wang, Rongliang, Niu, Ling, Xie, Chuanqi, Ding, Jian, Liao, Yongcui, Wang, Liyuan, Wan, Hongjiao, Ma, Guangqiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10406886/
https://www.ncbi.nlm.nih.gov/pubmed/37550359
http://dx.doi.org/10.1038/s41598-023-39665-7
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author Yan, Chenghua
Kuang, Wendong
Jin, Liang
Wang, Rongliang
Niu, Ling
Xie, Chuanqi
Ding, Jian
Liao, Yongcui
Wang, Liyuan
Wan, Hongjiao
Ma, Guangqiang
author_facet Yan, Chenghua
Kuang, Wendong
Jin, Liang
Wang, Rongliang
Niu, Ling
Xie, Chuanqi
Ding, Jian
Liao, Yongcui
Wang, Liyuan
Wan, Hongjiao
Ma, Guangqiang
author_sort Yan, Chenghua
collection PubMed
description Macrophages play an important role in the development of life-threatening sepsis, which is characterized by multiorgan dysfunction, through their ability to produce inflammatory cytokines. Carvacrol is a phenolic compound that has been confirmed to possess strong anti‑inflammatory activity. In this study, we mainly investigated the effect of carvacrol on lipopolysaccharide (LPS)-induced macrophage proinflammatory responses and endotoxic shock. The results showed that carvacrol significantly reduced mouse body weight loss and ameliorated pathological damage to the liver, lung, and heart under LPS-induced sepsis. Carvacrol attenuated inflammatory responses by inhibiting the LPS-induced production of inflammatory cytokine interleukin-6 (IL-6) in vivo and in vitro. Mechanistically, carvacrol inhibited IL-6 production mainly through the ERK1/2 signalling pathway in macrophages. Furthermore, carvacrol improved the survival of septic mice. This study sheds light on the role of carvacrol in the pathogenesis of LPS-induced sepsis, and thus, its potential in treating sepsis patients may be considered.
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spelling pubmed-104068862023-08-09 Carvacrol protects mice against LPS-induced sepsis and attenuates inflammatory response in macrophages by modulating the ERK1/2 pathway Yan, Chenghua Kuang, Wendong Jin, Liang Wang, Rongliang Niu, Ling Xie, Chuanqi Ding, Jian Liao, Yongcui Wang, Liyuan Wan, Hongjiao Ma, Guangqiang Sci Rep Article Macrophages play an important role in the development of life-threatening sepsis, which is characterized by multiorgan dysfunction, through their ability to produce inflammatory cytokines. Carvacrol is a phenolic compound that has been confirmed to possess strong anti‑inflammatory activity. In this study, we mainly investigated the effect of carvacrol on lipopolysaccharide (LPS)-induced macrophage proinflammatory responses and endotoxic shock. The results showed that carvacrol significantly reduced mouse body weight loss and ameliorated pathological damage to the liver, lung, and heart under LPS-induced sepsis. Carvacrol attenuated inflammatory responses by inhibiting the LPS-induced production of inflammatory cytokine interleukin-6 (IL-6) in vivo and in vitro. Mechanistically, carvacrol inhibited IL-6 production mainly through the ERK1/2 signalling pathway in macrophages. Furthermore, carvacrol improved the survival of septic mice. This study sheds light on the role of carvacrol in the pathogenesis of LPS-induced sepsis, and thus, its potential in treating sepsis patients may be considered. Nature Publishing Group UK 2023-08-07 /pmc/articles/PMC10406886/ /pubmed/37550359 http://dx.doi.org/10.1038/s41598-023-39665-7 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Yan, Chenghua
Kuang, Wendong
Jin, Liang
Wang, Rongliang
Niu, Ling
Xie, Chuanqi
Ding, Jian
Liao, Yongcui
Wang, Liyuan
Wan, Hongjiao
Ma, Guangqiang
Carvacrol protects mice against LPS-induced sepsis and attenuates inflammatory response in macrophages by modulating the ERK1/2 pathway
title Carvacrol protects mice against LPS-induced sepsis and attenuates inflammatory response in macrophages by modulating the ERK1/2 pathway
title_full Carvacrol protects mice against LPS-induced sepsis and attenuates inflammatory response in macrophages by modulating the ERK1/2 pathway
title_fullStr Carvacrol protects mice against LPS-induced sepsis and attenuates inflammatory response in macrophages by modulating the ERK1/2 pathway
title_full_unstemmed Carvacrol protects mice against LPS-induced sepsis and attenuates inflammatory response in macrophages by modulating the ERK1/2 pathway
title_short Carvacrol protects mice against LPS-induced sepsis and attenuates inflammatory response in macrophages by modulating the ERK1/2 pathway
title_sort carvacrol protects mice against lps-induced sepsis and attenuates inflammatory response in macrophages by modulating the erk1/2 pathway
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10406886/
https://www.ncbi.nlm.nih.gov/pubmed/37550359
http://dx.doi.org/10.1038/s41598-023-39665-7
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