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Huang Qi Tong Bi Decoction Attenuates Myocardial Ischemia-Reperfusion Injury via HMGB1/TLR/NF-κB Pathway

The aim of this study was to study the protective effect of Huang Qi Tong Bi Decoction (HQTBT) on the heart of rats. Ischemia-reperfusion injury was established by coronary artery ligation. Proinflammatory cytokines were decreased by XFZY in coronary artery ligated rats. ST segment was also restored...

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Detalles Bibliográficos
Autores principales: Liu, Kun, Li, Manman, Ren, Xiumei, You, Qing-sheng, Wang, Fei, Wang, Shuo, Ma, Chun-Hui, Li, Wei-Nan, Ye, Qing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6421754/
https://www.ncbi.nlm.nih.gov/pubmed/30944548
http://dx.doi.org/10.1155/2019/8387636
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author Liu, Kun
Li, Manman
Ren, Xiumei
You, Qing-sheng
Wang, Fei
Wang, Shuo
Ma, Chun-Hui
Li, Wei-Nan
Ye, Qing
author_facet Liu, Kun
Li, Manman
Ren, Xiumei
You, Qing-sheng
Wang, Fei
Wang, Shuo
Ma, Chun-Hui
Li, Wei-Nan
Ye, Qing
author_sort Liu, Kun
collection PubMed
description The aim of this study was to study the protective effect of Huang Qi Tong Bi Decoction (HQTBT) on the heart of rats. Ischemia-reperfusion injury was established by coronary artery ligation. Proinflammatory cytokines were decreased by XFZY in coronary artery ligated rats. ST segment was also restored with the treatment of HQTBT. Triphenyltetrazole chloride (TTC) staining and pathological analysis showed that HQTBT reduced myocardial injury. Besides, the expressions of HMGB1/TLR/NF-κB pathway in rats were significantly decreased by HQTBT. This study shows that HQTBT inhibited inflammatory reaction on myocardial injury in rats.
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spelling pubmed-64217542019-04-03 Huang Qi Tong Bi Decoction Attenuates Myocardial Ischemia-Reperfusion Injury via HMGB1/TLR/NF-κB Pathway Liu, Kun Li, Manman Ren, Xiumei You, Qing-sheng Wang, Fei Wang, Shuo Ma, Chun-Hui Li, Wei-Nan Ye, Qing Mediators Inflamm Research Article The aim of this study was to study the protective effect of Huang Qi Tong Bi Decoction (HQTBT) on the heart of rats. Ischemia-reperfusion injury was established by coronary artery ligation. Proinflammatory cytokines were decreased by XFZY in coronary artery ligated rats. ST segment was also restored with the treatment of HQTBT. Triphenyltetrazole chloride (TTC) staining and pathological analysis showed that HQTBT reduced myocardial injury. Besides, the expressions of HMGB1/TLR/NF-κB pathway in rats were significantly decreased by HQTBT. This study shows that HQTBT inhibited inflammatory reaction on myocardial injury in rats. Hindawi 2019-03-03 /pmc/articles/PMC6421754/ /pubmed/30944548 http://dx.doi.org/10.1155/2019/8387636 Text en Copyright © 2019 Kun Liu et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Liu, Kun
Li, Manman
Ren, Xiumei
You, Qing-sheng
Wang, Fei
Wang, Shuo
Ma, Chun-Hui
Li, Wei-Nan
Ye, Qing
Huang Qi Tong Bi Decoction Attenuates Myocardial Ischemia-Reperfusion Injury via HMGB1/TLR/NF-κB Pathway
title Huang Qi Tong Bi Decoction Attenuates Myocardial Ischemia-Reperfusion Injury via HMGB1/TLR/NF-κB Pathway
title_full Huang Qi Tong Bi Decoction Attenuates Myocardial Ischemia-Reperfusion Injury via HMGB1/TLR/NF-κB Pathway
title_fullStr Huang Qi Tong Bi Decoction Attenuates Myocardial Ischemia-Reperfusion Injury via HMGB1/TLR/NF-κB Pathway
title_full_unstemmed Huang Qi Tong Bi Decoction Attenuates Myocardial Ischemia-Reperfusion Injury via HMGB1/TLR/NF-κB Pathway
title_short Huang Qi Tong Bi Decoction Attenuates Myocardial Ischemia-Reperfusion Injury via HMGB1/TLR/NF-κB Pathway
title_sort huang qi tong bi decoction attenuates myocardial ischemia-reperfusion injury via hmgb1/tlr/nf-κb pathway
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6421754/
https://www.ncbi.nlm.nih.gov/pubmed/30944548
http://dx.doi.org/10.1155/2019/8387636
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