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Yiqi Fumai lyophilized injection attenuates doxorubicin-induced cardiotoxicity, hepatotoxicity and nephrotoxicity in rats by inhibition of oxidative stress, inflammation and apoptosis
Doxorubicin (DOX) is one of the most effective antineoplastic drugs, however, its organ toxicity inhibits the clinical utility. This study was aimed at investigating the protective effects of Yiqi Fumai lyophilized injection (YQFM) against DOX-induced tissue injury and exploring the mechanisms which...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Royal Society of Chemistry
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9091596/ https://www.ncbi.nlm.nih.gov/pubmed/35557896 http://dx.doi.org/10.1039/c8ra07163b |
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author | Gu, Yue Ju, Aichun Jiang, Bingjie Zhang, Jingze Man, Shuli Liu, Changxiao Gao, Wenyuan |
author_facet | Gu, Yue Ju, Aichun Jiang, Bingjie Zhang, Jingze Man, Shuli Liu, Changxiao Gao, Wenyuan |
author_sort | Gu, Yue |
collection | PubMed |
description | Doxorubicin (DOX) is one of the most effective antineoplastic drugs, however, its organ toxicity inhibits the clinical utility. This study was aimed at investigating the protective effects of Yiqi Fumai lyophilized injection (YQFM) against DOX-induced tissue injury and exploring the mechanisms which mediated reactive oxygen species (ROS), inflammation and apoptosis. The experiment was as follows: rats were subjected to an intraperitoneal injection (i.p.) of YQFM (0.481 g kg(−1), i.p.) for 12 days; DOX (5 mg kg(−1), i.p.) was administered on the 4th, 8th and 12th days to achieve a cumulative dose of 15 mg kg(−1). Pretreatment of YQFM significantly ameliorated intracellular damage and dysfunction of the heart, liver and kidneys via decreasing activities of injury indexes. The levels of lipid peroxidation and glutathione depletion were clearly reduced following YQFM pretreatment, meanwhile the activities of glutathione peroxidase, superoxide dismutase, and catalase were elevated. Additionally administering YQFM could mitigate the cardiotoxicity, hepatotoxicity and nephrotoxicity via reducing levels of inflammatory factors and decreasing apoptosis. Accordingly, this study indicated that YQFM attenuated DOX-induced toxicity by ameliorating organ function, decreasing ROS production, and preventing excessive inflammation and apoptosis. |
format | Online Article Text |
id | pubmed-9091596 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | The Royal Society of Chemistry |
record_format | MEDLINE/PubMed |
spelling | pubmed-90915962022-05-11 Yiqi Fumai lyophilized injection attenuates doxorubicin-induced cardiotoxicity, hepatotoxicity and nephrotoxicity in rats by inhibition of oxidative stress, inflammation and apoptosis Gu, Yue Ju, Aichun Jiang, Bingjie Zhang, Jingze Man, Shuli Liu, Changxiao Gao, Wenyuan RSC Adv Chemistry Doxorubicin (DOX) is one of the most effective antineoplastic drugs, however, its organ toxicity inhibits the clinical utility. This study was aimed at investigating the protective effects of Yiqi Fumai lyophilized injection (YQFM) against DOX-induced tissue injury and exploring the mechanisms which mediated reactive oxygen species (ROS), inflammation and apoptosis. The experiment was as follows: rats were subjected to an intraperitoneal injection (i.p.) of YQFM (0.481 g kg(−1), i.p.) for 12 days; DOX (5 mg kg(−1), i.p.) was administered on the 4th, 8th and 12th days to achieve a cumulative dose of 15 mg kg(−1). Pretreatment of YQFM significantly ameliorated intracellular damage and dysfunction of the heart, liver and kidneys via decreasing activities of injury indexes. The levels of lipid peroxidation and glutathione depletion were clearly reduced following YQFM pretreatment, meanwhile the activities of glutathione peroxidase, superoxide dismutase, and catalase were elevated. Additionally administering YQFM could mitigate the cardiotoxicity, hepatotoxicity and nephrotoxicity via reducing levels of inflammatory factors and decreasing apoptosis. Accordingly, this study indicated that YQFM attenuated DOX-induced toxicity by ameliorating organ function, decreasing ROS production, and preventing excessive inflammation and apoptosis. The Royal Society of Chemistry 2018-12-06 /pmc/articles/PMC9091596/ /pubmed/35557896 http://dx.doi.org/10.1039/c8ra07163b Text en This journal is © The Royal Society of Chemistry https://creativecommons.org/licenses/by-nc/3.0/ |
spellingShingle | Chemistry Gu, Yue Ju, Aichun Jiang, Bingjie Zhang, Jingze Man, Shuli Liu, Changxiao Gao, Wenyuan Yiqi Fumai lyophilized injection attenuates doxorubicin-induced cardiotoxicity, hepatotoxicity and nephrotoxicity in rats by inhibition of oxidative stress, inflammation and apoptosis |
title | Yiqi Fumai lyophilized injection attenuates doxorubicin-induced cardiotoxicity, hepatotoxicity and nephrotoxicity in rats by inhibition of oxidative stress, inflammation and apoptosis |
title_full | Yiqi Fumai lyophilized injection attenuates doxorubicin-induced cardiotoxicity, hepatotoxicity and nephrotoxicity in rats by inhibition of oxidative stress, inflammation and apoptosis |
title_fullStr | Yiqi Fumai lyophilized injection attenuates doxorubicin-induced cardiotoxicity, hepatotoxicity and nephrotoxicity in rats by inhibition of oxidative stress, inflammation and apoptosis |
title_full_unstemmed | Yiqi Fumai lyophilized injection attenuates doxorubicin-induced cardiotoxicity, hepatotoxicity and nephrotoxicity in rats by inhibition of oxidative stress, inflammation and apoptosis |
title_short | Yiqi Fumai lyophilized injection attenuates doxorubicin-induced cardiotoxicity, hepatotoxicity and nephrotoxicity in rats by inhibition of oxidative stress, inflammation and apoptosis |
title_sort | yiqi fumai lyophilized injection attenuates doxorubicin-induced cardiotoxicity, hepatotoxicity and nephrotoxicity in rats by inhibition of oxidative stress, inflammation and apoptosis |
topic | Chemistry |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9091596/ https://www.ncbi.nlm.nih.gov/pubmed/35557896 http://dx.doi.org/10.1039/c8ra07163b |
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