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Effects of trimetazidine on mitochondrial respiratory function, biosynthesis, and fission/fusion in rats with acute myocardial ischemia
OBJECTIVE: Myocardial ischemia affects mitochondrial functions, leading to ionic imbalance and susceptibility to ventricular fibrillation. Trimetazidine, a metabolic agent, is clinically used in anti-anginal therapy. METHODS: In this study, the rats were orally treated by gavage with trimetazidine 1...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Kare Publishing
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5689048/ https://www.ncbi.nlm.nih.gov/pubmed/28761019 http://dx.doi.org/10.14744/AnatolJCardiol.2017.7771 |
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author | Shi, Wen Shangguan, Wenfeng Zhang, Yue Li, Can Li, Guangping |
author_facet | Shi, Wen Shangguan, Wenfeng Zhang, Yue Li, Can Li, Guangping |
author_sort | Shi, Wen |
collection | PubMed |
description | OBJECTIVE: Myocardial ischemia affects mitochondrial functions, leading to ionic imbalance and susceptibility to ventricular fibrillation. Trimetazidine, a metabolic agent, is clinically used in anti-anginal therapy. METHODS: In this study, the rats were orally treated by gavage with trimetazidine 10 mg/kg/d for 7 days, and the effects of trimetazidine on mitochondrial respiratory function, biosynthesis, and fission/fusion in rats with acute myocardial ischemia were evaluated. RESULTS: It has been suggested that acute myocardial ischemia leads to a damage to mitochondrial functions. However, compared with ischemia group without trimetazidine administration, a significant reduction in the infarct size was observed in trimetazidine-treated ischemia group (31.24±3.02% vs. 52.87±4.89%). Trimetazidine preserved the mitochondrial structure and improved respiratory control ratio and complex I activity. Furthermore, trimetazidine improved mitochondrial biosynthesis and fission/fusion, as demonstrated by the promotion of peroxisome prolifera-tor-activated receptor gamma (PPARg) co-activator 1a (PGC-1a), mitofusins 1 (Mfn1), dynamin-related protein 1 (Drp1), and optic atrophy 1 (Opa1) expressions in rats with acute myocardial ischemia. CONCLUSION: Taken together, it was suggested that in this rat model of myocardial ischemia, trimetazidine demonstrated cardioprotective effects attributing to the preservation of mitochondrial respiratory function, biosynthesis, and fission/fusion and, thus, could be considered as an agent for cardioprotection. |
format | Online Article Text |
id | pubmed-5689048 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Kare Publishing |
record_format | MEDLINE/PubMed |
spelling | pubmed-56890482017-11-21 Effects of trimetazidine on mitochondrial respiratory function, biosynthesis, and fission/fusion in rats with acute myocardial ischemia Shi, Wen Shangguan, Wenfeng Zhang, Yue Li, Can Li, Guangping Anatol J Cardiol Original Investigation OBJECTIVE: Myocardial ischemia affects mitochondrial functions, leading to ionic imbalance and susceptibility to ventricular fibrillation. Trimetazidine, a metabolic agent, is clinically used in anti-anginal therapy. METHODS: In this study, the rats were orally treated by gavage with trimetazidine 10 mg/kg/d for 7 days, and the effects of trimetazidine on mitochondrial respiratory function, biosynthesis, and fission/fusion in rats with acute myocardial ischemia were evaluated. RESULTS: It has been suggested that acute myocardial ischemia leads to a damage to mitochondrial functions. However, compared with ischemia group without trimetazidine administration, a significant reduction in the infarct size was observed in trimetazidine-treated ischemia group (31.24±3.02% vs. 52.87±4.89%). Trimetazidine preserved the mitochondrial structure and improved respiratory control ratio and complex I activity. Furthermore, trimetazidine improved mitochondrial biosynthesis and fission/fusion, as demonstrated by the promotion of peroxisome prolifera-tor-activated receptor gamma (PPARg) co-activator 1a (PGC-1a), mitofusins 1 (Mfn1), dynamin-related protein 1 (Drp1), and optic atrophy 1 (Opa1) expressions in rats with acute myocardial ischemia. CONCLUSION: Taken together, it was suggested that in this rat model of myocardial ischemia, trimetazidine demonstrated cardioprotective effects attributing to the preservation of mitochondrial respiratory function, biosynthesis, and fission/fusion and, thus, could be considered as an agent for cardioprotection. Kare Publishing 2017-09 2017-07-25 /pmc/articles/PMC5689048/ /pubmed/28761019 http://dx.doi.org/10.14744/AnatolJCardiol.2017.7771 Text en Copyright: © 2017 Turkish Society of Cardiology http://creativecommons.org/licenses/by-nc-sa/4.0 This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License |
spellingShingle | Original Investigation Shi, Wen Shangguan, Wenfeng Zhang, Yue Li, Can Li, Guangping Effects of trimetazidine on mitochondrial respiratory function, biosynthesis, and fission/fusion in rats with acute myocardial ischemia |
title | Effects of trimetazidine on mitochondrial respiratory function, biosynthesis, and fission/fusion in rats with acute myocardial ischemia |
title_full | Effects of trimetazidine on mitochondrial respiratory function, biosynthesis, and fission/fusion in rats with acute myocardial ischemia |
title_fullStr | Effects of trimetazidine on mitochondrial respiratory function, biosynthesis, and fission/fusion in rats with acute myocardial ischemia |
title_full_unstemmed | Effects of trimetazidine on mitochondrial respiratory function, biosynthesis, and fission/fusion in rats with acute myocardial ischemia |
title_short | Effects of trimetazidine on mitochondrial respiratory function, biosynthesis, and fission/fusion in rats with acute myocardial ischemia |
title_sort | effects of trimetazidine on mitochondrial respiratory function, biosynthesis, and fission/fusion in rats with acute myocardial ischemia |
topic | Original Investigation |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5689048/ https://www.ncbi.nlm.nih.gov/pubmed/28761019 http://dx.doi.org/10.14744/AnatolJCardiol.2017.7771 |
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