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Tussilagone Inhibits the Inflammatory Response and Improves Survival in CLP-Induced Septic Mice

Tussilagone, extracted from Tussilago farfara is an oriental medicine used for asthma and bronchitis. We investigated its mechanism of action, its inhibitory effects on lipopolysaccharide-induced inflammation in macrophages, and its impact on viability in a cecal ligation and puncture (CLP)-induced...

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Autores principales: Kim, Yun Kyu, Yeo, Myeong Gu, Oh, Bo Kang, Kim, Ha Yeong, Yang, Hun Ji, Cho, Seung-Sik, Gil, Minchan, Lee, Kyung Jin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5751343/
https://www.ncbi.nlm.nih.gov/pubmed/29258263
http://dx.doi.org/10.3390/ijms18122744
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author Kim, Yun Kyu
Yeo, Myeong Gu
Oh, Bo Kang
Kim, Ha Yeong
Yang, Hun Ji
Cho, Seung-Sik
Gil, Minchan
Lee, Kyung Jin
author_facet Kim, Yun Kyu
Yeo, Myeong Gu
Oh, Bo Kang
Kim, Ha Yeong
Yang, Hun Ji
Cho, Seung-Sik
Gil, Minchan
Lee, Kyung Jin
author_sort Kim, Yun Kyu
collection PubMed
description Tussilagone, extracted from Tussilago farfara is an oriental medicine used for asthma and bronchitis. We investigated its mechanism of action, its inhibitory effects on lipopolysaccharide-induced inflammation in macrophages, and its impact on viability in a cecal ligation and puncture (CLP)-induced mouse model of sepsis. Tussilagone suppressed the expression of the inflammatory mediators, nitric oxide and prostaglandin E2, and the inflammatory cytokines, tumor necrosis factor-alpha (TNF-α) and high-mobility group box 1 (HMGB1), in lipopolysaccharide-stimulated RAW 264.7 cells and peritoneal macrophages. Tussilagone also reduced the activation of the mitogen-activated protein kinases and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) involved in the activation of various inflammatory mediators in activated macrophages. Moreover, tussilagone administration (1 mg/kg and 10 mg/kg) produced decreased mortality and lung injury in CLP-activated septic mice. Augmented expression of cyclooxygenase (COX)-2 and TNF-α in pulmonary alveolar macrophages of septic mice were attenuated by tussilagone administration. Tussilagone also suppressed the induction of nitric oxide, prostaglandin E2, TNF-α and HMGB1 in the serum of the septic mice. Overall, tussilagone exhibited protective effects against inflammation and polymicrobial sepsis by suppressing inflammatory mediators possibly via the inhibition of NF-κB activation and the MAP kinase pathway. These results suggest the possible use of tussilagone for developing novel therapeutic modalities for sepsis and other inflammatory diseases.
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spelling pubmed-57513432018-01-08 Tussilagone Inhibits the Inflammatory Response and Improves Survival in CLP-Induced Septic Mice Kim, Yun Kyu Yeo, Myeong Gu Oh, Bo Kang Kim, Ha Yeong Yang, Hun Ji Cho, Seung-Sik Gil, Minchan Lee, Kyung Jin Int J Mol Sci Article Tussilagone, extracted from Tussilago farfara is an oriental medicine used for asthma and bronchitis. We investigated its mechanism of action, its inhibitory effects on lipopolysaccharide-induced inflammation in macrophages, and its impact on viability in a cecal ligation and puncture (CLP)-induced mouse model of sepsis. Tussilagone suppressed the expression of the inflammatory mediators, nitric oxide and prostaglandin E2, and the inflammatory cytokines, tumor necrosis factor-alpha (TNF-α) and high-mobility group box 1 (HMGB1), in lipopolysaccharide-stimulated RAW 264.7 cells and peritoneal macrophages. Tussilagone also reduced the activation of the mitogen-activated protein kinases and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) involved in the activation of various inflammatory mediators in activated macrophages. Moreover, tussilagone administration (1 mg/kg and 10 mg/kg) produced decreased mortality and lung injury in CLP-activated septic mice. Augmented expression of cyclooxygenase (COX)-2 and TNF-α in pulmonary alveolar macrophages of septic mice were attenuated by tussilagone administration. Tussilagone also suppressed the induction of nitric oxide, prostaglandin E2, TNF-α and HMGB1 in the serum of the septic mice. Overall, tussilagone exhibited protective effects against inflammation and polymicrobial sepsis by suppressing inflammatory mediators possibly via the inhibition of NF-κB activation and the MAP kinase pathway. These results suggest the possible use of tussilagone for developing novel therapeutic modalities for sepsis and other inflammatory diseases. MDPI 2017-12-18 /pmc/articles/PMC5751343/ /pubmed/29258263 http://dx.doi.org/10.3390/ijms18122744 Text en © 2017 by the authors. 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 (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Kim, Yun Kyu
Yeo, Myeong Gu
Oh, Bo Kang
Kim, Ha Yeong
Yang, Hun Ji
Cho, Seung-Sik
Gil, Minchan
Lee, Kyung Jin
Tussilagone Inhibits the Inflammatory Response and Improves Survival in CLP-Induced Septic Mice
title Tussilagone Inhibits the Inflammatory Response and Improves Survival in CLP-Induced Septic Mice
title_full Tussilagone Inhibits the Inflammatory Response and Improves Survival in CLP-Induced Septic Mice
title_fullStr Tussilagone Inhibits the Inflammatory Response and Improves Survival in CLP-Induced Septic Mice
title_full_unstemmed Tussilagone Inhibits the Inflammatory Response and Improves Survival in CLP-Induced Septic Mice
title_short Tussilagone Inhibits the Inflammatory Response and Improves Survival in CLP-Induced Septic Mice
title_sort tussilagone inhibits the inflammatory response and improves survival in clp-induced septic mice
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5751343/
https://www.ncbi.nlm.nih.gov/pubmed/29258263
http://dx.doi.org/10.3390/ijms18122744
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