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QiShenYiQi Pills, a Compound Chinese Medicine, Prevented Cisplatin Induced Acute Kidney Injury via Regulating Mitochondrial Function
Nephrotoxicity is a serious adverse effect of cisplatin chemotherapy that limits its clinical application, to deal with which no effective management is available so far. The present study was to investigate the potential protective effect of QiShenYiQi Pills (QSYQ), a compound Chinese medicine, aga...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2017
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5743021/ https://www.ncbi.nlm.nih.gov/pubmed/29312001 http://dx.doi.org/10.3389/fphys.2017.01090 |
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author | Zhou, Li Wei, Xiao-Hong Pan, Chun-Shui Yan, Li Gu, You-Yu Sun, Kai Liu, Yu-Ying Wang, Chuan-She Fan, Jing-Yu Han, Jing-Yan |
author_facet | Zhou, Li Wei, Xiao-Hong Pan, Chun-Shui Yan, Li Gu, You-Yu Sun, Kai Liu, Yu-Ying Wang, Chuan-She Fan, Jing-Yu Han, Jing-Yan |
author_sort | Zhou, Li |
collection | PubMed |
description | Nephrotoxicity is a serious adverse effect of cisplatin chemotherapy that limits its clinical application, to deal with which no effective management is available so far. The present study was to investigate the potential protective effect of QiShenYiQi Pills (QSYQ), a compound Chinese medicine, against cisplatin induced nephrotoxicity in mice. Pretreatment with QSYQ significantly attenuated the cisplatin induced increase in plasma urea and creatinine, along with the histological damage, such as tubular necrosis, protein cast, and desquamation of epithelial cells, improved the renal microcirculation disturbance as indicated by renal blood flow, microvascular flow velocity, and the number of adherent leukocytes. Additionally, QSYQ prevented mitochondrial dysfunction by preventing the cisplatin induced downregulation of mitochondrial complex activity and the expression of NDUFA10, ATP5D, and Sirt3. Meanwhile, the cisplatin-increased renal thiobarbituric acid-reactive substances, caspase9, cleaved-caspase9, and cleaved-caspase3 were all diminished by QSYQ pretreatment. In summary, the pretreatment with QSYQ remarkably ameliorated the cisplatin induced nephrotoxicity in mice, possibly via the regulation of mitochondrial function, oxidative stress, and apoptosis. |
format | Online Article Text |
id | pubmed-5743021 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-57430212018-01-08 QiShenYiQi Pills, a Compound Chinese Medicine, Prevented Cisplatin Induced Acute Kidney Injury via Regulating Mitochondrial Function Zhou, Li Wei, Xiao-Hong Pan, Chun-Shui Yan, Li Gu, You-Yu Sun, Kai Liu, Yu-Ying Wang, Chuan-She Fan, Jing-Yu Han, Jing-Yan Front Physiol Physiology Nephrotoxicity is a serious adverse effect of cisplatin chemotherapy that limits its clinical application, to deal with which no effective management is available so far. The present study was to investigate the potential protective effect of QiShenYiQi Pills (QSYQ), a compound Chinese medicine, against cisplatin induced nephrotoxicity in mice. Pretreatment with QSYQ significantly attenuated the cisplatin induced increase in plasma urea and creatinine, along with the histological damage, such as tubular necrosis, protein cast, and desquamation of epithelial cells, improved the renal microcirculation disturbance as indicated by renal blood flow, microvascular flow velocity, and the number of adherent leukocytes. Additionally, QSYQ prevented mitochondrial dysfunction by preventing the cisplatin induced downregulation of mitochondrial complex activity and the expression of NDUFA10, ATP5D, and Sirt3. Meanwhile, the cisplatin-increased renal thiobarbituric acid-reactive substances, caspase9, cleaved-caspase9, and cleaved-caspase3 were all diminished by QSYQ pretreatment. In summary, the pretreatment with QSYQ remarkably ameliorated the cisplatin induced nephrotoxicity in mice, possibly via the regulation of mitochondrial function, oxidative stress, and apoptosis. Frontiers Media S.A. 2017-12-21 /pmc/articles/PMC5743021/ /pubmed/29312001 http://dx.doi.org/10.3389/fphys.2017.01090 Text en Copyright © 2017 Zhou, Wei, Pan, Yan, Gu, Sun, Liu, Wang, Fan and Han. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Physiology Zhou, Li Wei, Xiao-Hong Pan, Chun-Shui Yan, Li Gu, You-Yu Sun, Kai Liu, Yu-Ying Wang, Chuan-She Fan, Jing-Yu Han, Jing-Yan QiShenYiQi Pills, a Compound Chinese Medicine, Prevented Cisplatin Induced Acute Kidney Injury via Regulating Mitochondrial Function |
title | QiShenYiQi Pills, a Compound Chinese Medicine, Prevented Cisplatin Induced Acute Kidney Injury via Regulating Mitochondrial Function |
title_full | QiShenYiQi Pills, a Compound Chinese Medicine, Prevented Cisplatin Induced Acute Kidney Injury via Regulating Mitochondrial Function |
title_fullStr | QiShenYiQi Pills, a Compound Chinese Medicine, Prevented Cisplatin Induced Acute Kidney Injury via Regulating Mitochondrial Function |
title_full_unstemmed | QiShenYiQi Pills, a Compound Chinese Medicine, Prevented Cisplatin Induced Acute Kidney Injury via Regulating Mitochondrial Function |
title_short | QiShenYiQi Pills, a Compound Chinese Medicine, Prevented Cisplatin Induced Acute Kidney Injury via Regulating Mitochondrial Function |
title_sort | qishenyiqi pills, a compound chinese medicine, prevented cisplatin induced acute kidney injury via regulating mitochondrial function |
topic | Physiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5743021/ https://www.ncbi.nlm.nih.gov/pubmed/29312001 http://dx.doi.org/10.3389/fphys.2017.01090 |
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