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Qizhi Jiangtang Jiaonang Improves Insulin Signaling and Reduces Inflammatory Cytokine Secretion and Reactive Oxygen Species Formation in Insulin Resistant HepG2 Cells

We analyzed the effects of a traditional Chinese medicine, Qizhi Jiangtang Jiaonang (QJJ), on insulin resistance (IR) in vitro. After an in vitro model of IR was established by treating human liver cancer cells (HepG2 cells) with palmitic acid, the cells were then treated with various concentrations...

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Autores principales: Zhang, Xiao-Tian, Yu, Chun-Jiang, Liu, Jian-Wei, Zhang, Yan-Ping, Zhang, Chao, Song, Chen-Xue, Xie, Jing-Shu, Sai, Jing-Ying, Zheng, Jing-Tong, Wang, Fang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4436462/
https://www.ncbi.nlm.nih.gov/pubmed/26074994
http://dx.doi.org/10.1155/2015/518639
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author Zhang, Xiao-Tian
Yu, Chun-Jiang
Liu, Jian-Wei
Zhang, Yan-Ping
Zhang, Chao
Song, Chen-Xue
Xie, Jing-Shu
Sai, Jing-Ying
Zheng, Jing-Tong
Wang, Fang
author_facet Zhang, Xiao-Tian
Yu, Chun-Jiang
Liu, Jian-Wei
Zhang, Yan-Ping
Zhang, Chao
Song, Chen-Xue
Xie, Jing-Shu
Sai, Jing-Ying
Zheng, Jing-Tong
Wang, Fang
author_sort Zhang, Xiao-Tian
collection PubMed
description We analyzed the effects of a traditional Chinese medicine, Qizhi Jiangtang Jiaonang (QJJ), on insulin resistance (IR) in vitro. After an in vitro model of IR was established by treating human liver cancer cells (HepG2 cells) with palmitic acid, the cells were then treated with various concentrations of QJJ. Treatment with 400 µM palmitic acid for 24 h induced IR in HepG2 cells. The survival rate for HepG2 cells in the IR group was significantly lower than that of the untreated control group (P < 0.001); however, QJJ restored HepG2 cell survival (P < 0.001). As compared with HepG2 cells in the IR group, QJJ at all doses analyzed significantly increased glucose consumption (all P < 0.05). Moreover, treatment with all the QJJ doses significantly reduced the mean intracellular reactive oxygen species levels as compared with the IR group (all P < 0.05). Furthermore, high-dose QJJ reduced both TNF-α and IL-6 levels as compared to the IR group (all P < 0.05). QJJ ameliorated the altered PI3K, GLUT4, and RAGE expression observed with IR. In conclusion, QJJ can improve IR in HepG2 cells, which may be mediated through the IRS-1/PI3K/GLUT4 signaling pathway as well as regulation of NF-κB-mediated inflammation and oxidative stress.
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spelling pubmed-44364622015-06-14 Qizhi Jiangtang Jiaonang Improves Insulin Signaling and Reduces Inflammatory Cytokine Secretion and Reactive Oxygen Species Formation in Insulin Resistant HepG2 Cells Zhang, Xiao-Tian Yu, Chun-Jiang Liu, Jian-Wei Zhang, Yan-Ping Zhang, Chao Song, Chen-Xue Xie, Jing-Shu Sai, Jing-Ying Zheng, Jing-Tong Wang, Fang Evid Based Complement Alternat Med Research Article We analyzed the effects of a traditional Chinese medicine, Qizhi Jiangtang Jiaonang (QJJ), on insulin resistance (IR) in vitro. After an in vitro model of IR was established by treating human liver cancer cells (HepG2 cells) with palmitic acid, the cells were then treated with various concentrations of QJJ. Treatment with 400 µM palmitic acid for 24 h induced IR in HepG2 cells. The survival rate for HepG2 cells in the IR group was significantly lower than that of the untreated control group (P < 0.001); however, QJJ restored HepG2 cell survival (P < 0.001). As compared with HepG2 cells in the IR group, QJJ at all doses analyzed significantly increased glucose consumption (all P < 0.05). Moreover, treatment with all the QJJ doses significantly reduced the mean intracellular reactive oxygen species levels as compared with the IR group (all P < 0.05). Furthermore, high-dose QJJ reduced both TNF-α and IL-6 levels as compared to the IR group (all P < 0.05). QJJ ameliorated the altered PI3K, GLUT4, and RAGE expression observed with IR. In conclusion, QJJ can improve IR in HepG2 cells, which may be mediated through the IRS-1/PI3K/GLUT4 signaling pathway as well as regulation of NF-κB-mediated inflammation and oxidative stress. Hindawi Publishing Corporation 2015 2015-05-05 /pmc/articles/PMC4436462/ /pubmed/26074994 http://dx.doi.org/10.1155/2015/518639 Text en Copyright © 2015 Xiao-Tian Zhang et al. https://creativecommons.org/licenses/by/3.0/ 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
Zhang, Xiao-Tian
Yu, Chun-Jiang
Liu, Jian-Wei
Zhang, Yan-Ping
Zhang, Chao
Song, Chen-Xue
Xie, Jing-Shu
Sai, Jing-Ying
Zheng, Jing-Tong
Wang, Fang
Qizhi Jiangtang Jiaonang Improves Insulin Signaling and Reduces Inflammatory Cytokine Secretion and Reactive Oxygen Species Formation in Insulin Resistant HepG2 Cells
title Qizhi Jiangtang Jiaonang Improves Insulin Signaling and Reduces Inflammatory Cytokine Secretion and Reactive Oxygen Species Formation in Insulin Resistant HepG2 Cells
title_full Qizhi Jiangtang Jiaonang Improves Insulin Signaling and Reduces Inflammatory Cytokine Secretion and Reactive Oxygen Species Formation in Insulin Resistant HepG2 Cells
title_fullStr Qizhi Jiangtang Jiaonang Improves Insulin Signaling and Reduces Inflammatory Cytokine Secretion and Reactive Oxygen Species Formation in Insulin Resistant HepG2 Cells
title_full_unstemmed Qizhi Jiangtang Jiaonang Improves Insulin Signaling and Reduces Inflammatory Cytokine Secretion and Reactive Oxygen Species Formation in Insulin Resistant HepG2 Cells
title_short Qizhi Jiangtang Jiaonang Improves Insulin Signaling and Reduces Inflammatory Cytokine Secretion and Reactive Oxygen Species Formation in Insulin Resistant HepG2 Cells
title_sort qizhi jiangtang jiaonang improves insulin signaling and reduces inflammatory cytokine secretion and reactive oxygen species formation in insulin resistant hepg2 cells
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4436462/
https://www.ncbi.nlm.nih.gov/pubmed/26074994
http://dx.doi.org/10.1155/2015/518639
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