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Huang-Lian-Jie-Du-Tang Protects Rats from Cardiac Damages Induced by Metabolic Disorder by Improving Inflammation-Mediated Insulin Resistance

Huang-lian-jie-du-tang (HLJDT), a traditional Chinese medicine, has been shown to improve insulin resistance (IR) induced by inflammation, a key event in the development of metabolic syndrome (MS). The present study aimed to investigate the protective effects of HLJDT on MS and explore the underlyin...

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Autores principales: Li, Chuan Bao, Li, Xiao Xing, Chen, Yu Guo, Gao, Hai Qing, Bu, Pei Li, Zhang, Yun, Ji, Xiao Ping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3695866/
https://www.ncbi.nlm.nih.gov/pubmed/23840732
http://dx.doi.org/10.1371/journal.pone.0067530
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author Li, Chuan Bao
Li, Xiao Xing
Chen, Yu Guo
Gao, Hai Qing
Bu, Pei Li
Zhang, Yun
Ji, Xiao Ping
author_facet Li, Chuan Bao
Li, Xiao Xing
Chen, Yu Guo
Gao, Hai Qing
Bu, Pei Li
Zhang, Yun
Ji, Xiao Ping
author_sort Li, Chuan Bao
collection PubMed
description Huang-lian-jie-du-tang (HLJDT), a traditional Chinese medicine, has been shown to improve insulin resistance (IR) induced by inflammation, a key event in the development of metabolic syndrome (MS). The present study aimed to investigate the protective effects of HLJDT on MS and explore the underlying mechanism. MS rats were established with obese-diets and treated with normal saline, aspirin or HLJDT. The myocardial lesions were identified by echocardiogram, transmission electron microscope, and Sirius-red staining. The inflammatory cytokines were measured by ELISA and real-time PCR. The activation of NF-κB, JNK, SOCS3, IRS1 and AKT in the heart was detected by immunohistochemistry and Western blot analysis. Compared with the controls, MS rats developed obvious obesity, hypertension, dyslipidemia, IR, inflammation, and cardiac damage. Moreover, phosphorylated IRS-1 at Ser307 was correlated with the activation of NF-κB, JNK and SOCS3 and the inhibition of AKT in the heart from MS rats. These data suggest that serine phosphorylation of IRS-1 in response to inflammation is mediated, in part, by NF-κB, JNK and SOCS3. Notably, HLJDT inhibited the activation of NF-κB and reduced serine phosphorylation of IRS-1. In summary, HLJDT protects myocardium from IR-mediated injury by inhibiting serine phosphorylation of IRS-1 in MS rats.
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spelling pubmed-36958662013-07-09 Huang-Lian-Jie-Du-Tang Protects Rats from Cardiac Damages Induced by Metabolic Disorder by Improving Inflammation-Mediated Insulin Resistance Li, Chuan Bao Li, Xiao Xing Chen, Yu Guo Gao, Hai Qing Bu, Pei Li Zhang, Yun Ji, Xiao Ping PLoS One Research Article Huang-lian-jie-du-tang (HLJDT), a traditional Chinese medicine, has been shown to improve insulin resistance (IR) induced by inflammation, a key event in the development of metabolic syndrome (MS). The present study aimed to investigate the protective effects of HLJDT on MS and explore the underlying mechanism. MS rats were established with obese-diets and treated with normal saline, aspirin or HLJDT. The myocardial lesions were identified by echocardiogram, transmission electron microscope, and Sirius-red staining. The inflammatory cytokines were measured by ELISA and real-time PCR. The activation of NF-κB, JNK, SOCS3, IRS1 and AKT in the heart was detected by immunohistochemistry and Western blot analysis. Compared with the controls, MS rats developed obvious obesity, hypertension, dyslipidemia, IR, inflammation, and cardiac damage. Moreover, phosphorylated IRS-1 at Ser307 was correlated with the activation of NF-κB, JNK and SOCS3 and the inhibition of AKT in the heart from MS rats. These data suggest that serine phosphorylation of IRS-1 in response to inflammation is mediated, in part, by NF-κB, JNK and SOCS3. Notably, HLJDT inhibited the activation of NF-κB and reduced serine phosphorylation of IRS-1. In summary, HLJDT protects myocardium from IR-mediated injury by inhibiting serine phosphorylation of IRS-1 in MS rats. Public Library of Science 2013-06-28 /pmc/articles/PMC3695866/ /pubmed/23840732 http://dx.doi.org/10.1371/journal.pone.0067530 Text en © 2013 Li et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Li, Chuan Bao
Li, Xiao Xing
Chen, Yu Guo
Gao, Hai Qing
Bu, Pei Li
Zhang, Yun
Ji, Xiao Ping
Huang-Lian-Jie-Du-Tang Protects Rats from Cardiac Damages Induced by Metabolic Disorder by Improving Inflammation-Mediated Insulin Resistance
title Huang-Lian-Jie-Du-Tang Protects Rats from Cardiac Damages Induced by Metabolic Disorder by Improving Inflammation-Mediated Insulin Resistance
title_full Huang-Lian-Jie-Du-Tang Protects Rats from Cardiac Damages Induced by Metabolic Disorder by Improving Inflammation-Mediated Insulin Resistance
title_fullStr Huang-Lian-Jie-Du-Tang Protects Rats from Cardiac Damages Induced by Metabolic Disorder by Improving Inflammation-Mediated Insulin Resistance
title_full_unstemmed Huang-Lian-Jie-Du-Tang Protects Rats from Cardiac Damages Induced by Metabolic Disorder by Improving Inflammation-Mediated Insulin Resistance
title_short Huang-Lian-Jie-Du-Tang Protects Rats from Cardiac Damages Induced by Metabolic Disorder by Improving Inflammation-Mediated Insulin Resistance
title_sort huang-lian-jie-du-tang protects rats from cardiac damages induced by metabolic disorder by improving inflammation-mediated insulin resistance
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3695866/
https://www.ncbi.nlm.nih.gov/pubmed/23840732
http://dx.doi.org/10.1371/journal.pone.0067530
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