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Corilagin ameliorates the extreme inflammatory status in sepsis through TLR4 signaling pathways

BACKGROUND: Sepsis is one of the serious disorders in clinical practice. Recent studies found toll-like receptors 4 (TLR4) played an important role in sepsis. In this study, we tried to find the influence of Corilagin on TLR4 signal pathways in vitro and in vivo. METHODS: The cellular and animal mod...

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Autores principales: Li, Hua-Rong, Liu, Jie, Zhang, Shu-Ling, Luo, Tao, Wu, Fei, Dong, Ji-Hua, Guo, Yuan-Jin, Zhao, Lei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5217594/
https://www.ncbi.nlm.nih.gov/pubmed/28056977
http://dx.doi.org/10.1186/s12906-016-1533-y
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author Li, Hua-Rong
Liu, Jie
Zhang, Shu-Ling
Luo, Tao
Wu, Fei
Dong, Ji-Hua
Guo, Yuan-Jin
Zhao, Lei
author_facet Li, Hua-Rong
Liu, Jie
Zhang, Shu-Ling
Luo, Tao
Wu, Fei
Dong, Ji-Hua
Guo, Yuan-Jin
Zhao, Lei
author_sort Li, Hua-Rong
collection PubMed
description BACKGROUND: Sepsis is one of the serious disorders in clinical practice. Recent studies found toll-like receptors 4 (TLR4) played an important role in sepsis. In this study, we tried to find the influence of Corilagin on TLR4 signal pathways in vitro and in vivo. METHODS: The cellular and animal models of sepsis were established by LPS and then interfered with Corilagin. Real-time PCR and western blot were employed to detect the mRNA and protein expressions of TLR4, MyD88, TRIF and TRAF6. ELISA was used to determine the IL-6 and IL-1β levels in supernatant and serum. RESULTS: The survival rate was improved in the LPS + Corilagin group, and the mRNA and protein expressions of TLR4, MyD88, TRIF and TRAF6 were significantly decreased than that in the LPS group both in cellular and animal models (P < 0.01). The pro-inflammatory cytokines IL-6 and IL-1β were greatly decreased in the LPS + Corilagin group both in supernatant and serum (P < 0.01). CONCLUSIONS: Corilagin exerts the anti-inflammatory effects by down-regulating the TLR4 signaling molecules to ameliorate the extreme inflammatory status in sepsis.
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spelling pubmed-52175942017-01-09 Corilagin ameliorates the extreme inflammatory status in sepsis through TLR4 signaling pathways Li, Hua-Rong Liu, Jie Zhang, Shu-Ling Luo, Tao Wu, Fei Dong, Ji-Hua Guo, Yuan-Jin Zhao, Lei BMC Complement Altern Med Research Article BACKGROUND: Sepsis is one of the serious disorders in clinical practice. Recent studies found toll-like receptors 4 (TLR4) played an important role in sepsis. In this study, we tried to find the influence of Corilagin on TLR4 signal pathways in vitro and in vivo. METHODS: The cellular and animal models of sepsis were established by LPS and then interfered with Corilagin. Real-time PCR and western blot were employed to detect the mRNA and protein expressions of TLR4, MyD88, TRIF and TRAF6. ELISA was used to determine the IL-6 and IL-1β levels in supernatant and serum. RESULTS: The survival rate was improved in the LPS + Corilagin group, and the mRNA and protein expressions of TLR4, MyD88, TRIF and TRAF6 were significantly decreased than that in the LPS group both in cellular and animal models (P < 0.01). The pro-inflammatory cytokines IL-6 and IL-1β were greatly decreased in the LPS + Corilagin group both in supernatant and serum (P < 0.01). CONCLUSIONS: Corilagin exerts the anti-inflammatory effects by down-regulating the TLR4 signaling molecules to ameliorate the extreme inflammatory status in sepsis. BioMed Central 2017-01-05 /pmc/articles/PMC5217594/ /pubmed/28056977 http://dx.doi.org/10.1186/s12906-016-1533-y Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Li, Hua-Rong
Liu, Jie
Zhang, Shu-Ling
Luo, Tao
Wu, Fei
Dong, Ji-Hua
Guo, Yuan-Jin
Zhao, Lei
Corilagin ameliorates the extreme inflammatory status in sepsis through TLR4 signaling pathways
title Corilagin ameliorates the extreme inflammatory status in sepsis through TLR4 signaling pathways
title_full Corilagin ameliorates the extreme inflammatory status in sepsis through TLR4 signaling pathways
title_fullStr Corilagin ameliorates the extreme inflammatory status in sepsis through TLR4 signaling pathways
title_full_unstemmed Corilagin ameliorates the extreme inflammatory status in sepsis through TLR4 signaling pathways
title_short Corilagin ameliorates the extreme inflammatory status in sepsis through TLR4 signaling pathways
title_sort corilagin ameliorates the extreme inflammatory status in sepsis through tlr4 signaling pathways
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5217594/
https://www.ncbi.nlm.nih.gov/pubmed/28056977
http://dx.doi.org/10.1186/s12906-016-1533-y
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