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Protective effect of berberine on acute cardiomyopathy associated with doxorubicin treatment
Doxorubicin (DOX) is a potent and broad-spectrum anthracycline chemotherapeutic agent, but dose-dependent cardiotoxic side effects limit its clinical application. This toxicity is closely associated with the generation of reactive oxygen species (ROS) radical during DOX metabolism. The present study...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5840547/ https://www.ncbi.nlm.nih.gov/pubmed/29552206 http://dx.doi.org/10.3892/ol.2018.8020 |
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author | Xiong, Chen Wu, Yan-Zhao Zhang, Yu Wu, Zi-Xiao Chen, Xue-Yan Jiang, Ping Guo, Hui-Cai Xie, Ke-Rang Wang, Ke-Xin Su, Su-Wen |
author_facet | Xiong, Chen Wu, Yan-Zhao Zhang, Yu Wu, Zi-Xiao Chen, Xue-Yan Jiang, Ping Guo, Hui-Cai Xie, Ke-Rang Wang, Ke-Xin Su, Su-Wen |
author_sort | Xiong, Chen |
collection | PubMed |
description | Doxorubicin (DOX) is a potent and broad-spectrum anthracycline chemotherapeutic agent, but dose-dependent cardiotoxic side effects limit its clinical application. This toxicity is closely associated with the generation of reactive oxygen species (ROS) radical during DOX metabolism. The present study investigated the effects of Berberine (Ber) on DOX-induced acute cardiac injury in a rat model and analysed its mechanism in cardiomyocytes in vitro. Serum creatine kinase (CK), creatine kinase isoenzyme (CK-MB) and malondialdehyde (MDA) levels were significantly increased in the DOX group compared with the control group. This increase was accompanied by cardiac histopathological injury and a decrease in cardiomyocyte superoxide dismutase (SOD) and catalase (CAT). CK, CK-MB and MDA levels decreased and SOD and CAT levels increased in the Ber-treated group compared to the DOX group. Ber ameliorated the DOX-induced increase in cytosolic calcium concentration ([Ca(2+)](i)), attenuated mitochondrial Ca(2+) overload and restored the DOX-induced loss of mitochondrial membrane potential in vitro. These results demonstrated that Ber exhibited protective effects against DOX-induced heart tissue free radical injury, potentially via the inhibition of intracellular Ca(2+) elevation and attenuation of mitochondrial dysfunction. |
format | Online Article Text |
id | pubmed-5840547 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-58405472018-03-16 Protective effect of berberine on acute cardiomyopathy associated with doxorubicin treatment Xiong, Chen Wu, Yan-Zhao Zhang, Yu Wu, Zi-Xiao Chen, Xue-Yan Jiang, Ping Guo, Hui-Cai Xie, Ke-Rang Wang, Ke-Xin Su, Su-Wen Oncol Lett Articles Doxorubicin (DOX) is a potent and broad-spectrum anthracycline chemotherapeutic agent, but dose-dependent cardiotoxic side effects limit its clinical application. This toxicity is closely associated with the generation of reactive oxygen species (ROS) radical during DOX metabolism. The present study investigated the effects of Berberine (Ber) on DOX-induced acute cardiac injury in a rat model and analysed its mechanism in cardiomyocytes in vitro. Serum creatine kinase (CK), creatine kinase isoenzyme (CK-MB) and malondialdehyde (MDA) levels were significantly increased in the DOX group compared with the control group. This increase was accompanied by cardiac histopathological injury and a decrease in cardiomyocyte superoxide dismutase (SOD) and catalase (CAT). CK, CK-MB and MDA levels decreased and SOD and CAT levels increased in the Ber-treated group compared to the DOX group. Ber ameliorated the DOX-induced increase in cytosolic calcium concentration ([Ca(2+)](i)), attenuated mitochondrial Ca(2+) overload and restored the DOX-induced loss of mitochondrial membrane potential in vitro. These results demonstrated that Ber exhibited protective effects against DOX-induced heart tissue free radical injury, potentially via the inhibition of intracellular Ca(2+) elevation and attenuation of mitochondrial dysfunction. D.A. Spandidos 2018-04 2018-02-09 /pmc/articles/PMC5840547/ /pubmed/29552206 http://dx.doi.org/10.3892/ol.2018.8020 Text en Copyright: © Xiong et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Xiong, Chen Wu, Yan-Zhao Zhang, Yu Wu, Zi-Xiao Chen, Xue-Yan Jiang, Ping Guo, Hui-Cai Xie, Ke-Rang Wang, Ke-Xin Su, Su-Wen Protective effect of berberine on acute cardiomyopathy associated with doxorubicin treatment |
title | Protective effect of berberine on acute cardiomyopathy associated with doxorubicin treatment |
title_full | Protective effect of berberine on acute cardiomyopathy associated with doxorubicin treatment |
title_fullStr | Protective effect of berberine on acute cardiomyopathy associated with doxorubicin treatment |
title_full_unstemmed | Protective effect of berberine on acute cardiomyopathy associated with doxorubicin treatment |
title_short | Protective effect of berberine on acute cardiomyopathy associated with doxorubicin treatment |
title_sort | protective effect of berberine on acute cardiomyopathy associated with doxorubicin treatment |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5840547/ https://www.ncbi.nlm.nih.gov/pubmed/29552206 http://dx.doi.org/10.3892/ol.2018.8020 |
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