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Lianqinjiedu decoction attenuates LPS-induced inflammation and acute lung injury in rats via TLR4/NF-κB pathway
Acute lung injury (ALI) and its severe form acute respiratory distress syndrome remain the leading cause of morbidity and mortality. LianQinJieDu (LQJD), which is a traditional Chinese medicine, has been clinically used for antiviral drug. The present study investigated whether Lianqinjiedu(LQJD) am...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier Masson SAS.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9678351/ https://www.ncbi.nlm.nih.gov/pubmed/28972887 http://dx.doi.org/10.1016/j.biopha.2017.09.094 |
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author | Deng, Guiming He, Hai Chen, Zheng OuYang, Linqi Xiao, Xiaoqin Ge, Jinwen Xiang, Biao Jiang, Sichen Cheng, Shaowu |
author_facet | Deng, Guiming He, Hai Chen, Zheng OuYang, Linqi Xiao, Xiaoqin Ge, Jinwen Xiang, Biao Jiang, Sichen Cheng, Shaowu |
author_sort | Deng, Guiming |
collection | PubMed |
description | Acute lung injury (ALI) and its severe form acute respiratory distress syndrome remain the leading cause of morbidity and mortality. LianQinJieDu (LQJD), which is a traditional Chinese medicine, has been clinically used for antiviral drug. The present study investigated whether Lianqinjiedu(LQJD) ameliorates lipopolysaccharide(LPS)-induced acute lung injury in rats and aimed to determine the anti-inflammatory effects of LQJD. Rat model with ALI induced by intraperitoneal injection of LPS was treated by oral administration of LQJD. The recruitment of body temperature and the histopathology of lung tissue from all groups were evaluated to grade the severity of the inflammation. The inflammatory cytokine levels, including tumor necrosis factor-α (TNF-α)and interleukin-6 (IL-6), were examined by ELISA assay, and the TLR4 and NF-κBp65 expression levels were evaluated by Real time-PCR and western blotting. It was observed that LQJD reduced the LPS-induced body temperature, inflammatory cytokines level, and lung injuries, and blocked the activation of TLR4/NF-κBp65 signaling in lung tissue. This study demonstrates that LQJD has a protective effect on LPS-induced inflammatory rats through the signaling pathway of TLR4 and NF-κBp65. |
format | Online Article Text |
id | pubmed-9678351 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Elsevier Masson SAS. |
record_format | MEDLINE/PubMed |
spelling | pubmed-96783512022-11-22 Lianqinjiedu decoction attenuates LPS-induced inflammation and acute lung injury in rats via TLR4/NF-κB pathway Deng, Guiming He, Hai Chen, Zheng OuYang, Linqi Xiao, Xiaoqin Ge, Jinwen Xiang, Biao Jiang, Sichen Cheng, Shaowu Biomed Pharmacother Article Acute lung injury (ALI) and its severe form acute respiratory distress syndrome remain the leading cause of morbidity and mortality. LianQinJieDu (LQJD), which is a traditional Chinese medicine, has been clinically used for antiviral drug. The present study investigated whether Lianqinjiedu(LQJD) ameliorates lipopolysaccharide(LPS)-induced acute lung injury in rats and aimed to determine the anti-inflammatory effects of LQJD. Rat model with ALI induced by intraperitoneal injection of LPS was treated by oral administration of LQJD. The recruitment of body temperature and the histopathology of lung tissue from all groups were evaluated to grade the severity of the inflammation. The inflammatory cytokine levels, including tumor necrosis factor-α (TNF-α)and interleukin-6 (IL-6), were examined by ELISA assay, and the TLR4 and NF-κBp65 expression levels were evaluated by Real time-PCR and western blotting. It was observed that LQJD reduced the LPS-induced body temperature, inflammatory cytokines level, and lung injuries, and blocked the activation of TLR4/NF-κBp65 signaling in lung tissue. This study demonstrates that LQJD has a protective effect on LPS-induced inflammatory rats through the signaling pathway of TLR4 and NF-κBp65. Elsevier Masson SAS. 2017-12 2017-09-30 /pmc/articles/PMC9678351/ /pubmed/28972887 http://dx.doi.org/10.1016/j.biopha.2017.09.094 Text en © 2017 Elsevier Masson SAS. All rights reserved. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active. |
spellingShingle | Article Deng, Guiming He, Hai Chen, Zheng OuYang, Linqi Xiao, Xiaoqin Ge, Jinwen Xiang, Biao Jiang, Sichen Cheng, Shaowu Lianqinjiedu decoction attenuates LPS-induced inflammation and acute lung injury in rats via TLR4/NF-κB pathway |
title | Lianqinjiedu decoction attenuates LPS-induced inflammation and acute lung injury in rats via TLR4/NF-κB pathway |
title_full | Lianqinjiedu decoction attenuates LPS-induced inflammation and acute lung injury in rats via TLR4/NF-κB pathway |
title_fullStr | Lianqinjiedu decoction attenuates LPS-induced inflammation and acute lung injury in rats via TLR4/NF-κB pathway |
title_full_unstemmed | Lianqinjiedu decoction attenuates LPS-induced inflammation and acute lung injury in rats via TLR4/NF-κB pathway |
title_short | Lianqinjiedu decoction attenuates LPS-induced inflammation and acute lung injury in rats via TLR4/NF-κB pathway |
title_sort | lianqinjiedu decoction attenuates lps-induced inflammation and acute lung injury in rats via tlr4/nf-κb pathway |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9678351/ https://www.ncbi.nlm.nih.gov/pubmed/28972887 http://dx.doi.org/10.1016/j.biopha.2017.09.094 |
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