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In vitro and in vivo study on prevention of myocardial ischemic injury by taurine

BACKGROUND: Myocardial ischemia (MI) often causes angina, arrhythmia, and cardiac insufficiency, sometimes resulting in death. Ischemia-induced myocardial tissue damage is attributed to the hypoxic damage of myocardial cells producing apoptosis and decreased proliferation. Taurine has been shown to...

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Autores principales: Ren, Fengyun, Liu, Xing, Liu, Xiaoxue, Cao, Yanli, Liu, Lantao, Li, Xingjiang, Wu, Yingjun, Du, Shudi, Tian, Guozhong, Hu, Jing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AME Publishing Company 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8267305/
https://www.ncbi.nlm.nih.gov/pubmed/34277784
http://dx.doi.org/10.21037/atm-21-2481
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author Ren, Fengyun
Liu, Xing
Liu, Xiaoxue
Cao, Yanli
Liu, Lantao
Li, Xingjiang
Wu, Yingjun
Du, Shudi
Tian, Guozhong
Hu, Jing
author_facet Ren, Fengyun
Liu, Xing
Liu, Xiaoxue
Cao, Yanli
Liu, Lantao
Li, Xingjiang
Wu, Yingjun
Du, Shudi
Tian, Guozhong
Hu, Jing
author_sort Ren, Fengyun
collection PubMed
description BACKGROUND: Myocardial ischemia (MI) often causes angina, arrhythmia, and cardiac insufficiency, sometimes resulting in death. Ischemia-induced myocardial tissue damage is attributed to the hypoxic damage of myocardial cells producing apoptosis and decreased proliferation. Taurine has been shown to improve MI, but its mechanism is largely unknown. METHODS: In this study, the relationship between taurine and severity of MI in vivo was evaluated by quantifying myocardial infarct areas and metabolic indicators of myocardial damage and measuring taurine levels in cardiac muscle and plasma by high performance liquid chromatography (HPLC). To elucidate how taurine might suppress ischemic injury, we established an in vitro ischemia model with isolated primary rat cardiomyocytes cultured without serum or glucose and under hypoxia. We evaluated the indicators of MI and damage, including lactic dehydrogenase (LDH), creatine kinase (CK), and cardiac troponin I (cTnI). We also examined the levels of taurine transporter (TauT), cysteine dioxygenase (CDO), and cysteine sulfinate decarboxylase (CSD) proteins involved in transport and synthesis of taurine in the myocardium and those of 2 apoptosis-associated proteins, namely, Bcl-2 associated X protein (BAX) and B-cell lymphoma-2 (Bcl-2). RESULTS: Exposure of myocardial cells to ischemia led to the decrease of taurine content, the suppression of cell proliferation, and led to calcium ion overload and apoptosis. Pretreatment with taurine alleviated the ischemic damage, with concomitant elevation of intracellular taurine concentrations. Molecular mechanism analysis showed that pretreatment with taurine upregulated the TauT, CDO, and CSD, 2 rate-limiting enzymes involved in taurine synthesis. These effects facilitated both taurine transport into cells and taurine synthesis, leading to taurine accumulation. In addition, apoptosis inhibition by taurine appeared to be mediated by upregulated Bcl-2 and downregulated BAX, as well as inhibition of calcium overload by suppression of calcium binding protein. CONCLUSIONS: We demonstrated that TauT is critical for the attenuation of myocardial ischemic damage by taurine, facilitating taurine absorption and synthesis. These findings provided new insights and a theoretical foundation for future studies examining taurine as a potential treatment for MI.
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spelling pubmed-82673052021-07-16 In vitro and in vivo study on prevention of myocardial ischemic injury by taurine Ren, Fengyun Liu, Xing Liu, Xiaoxue Cao, Yanli Liu, Lantao Li, Xingjiang Wu, Yingjun Du, Shudi Tian, Guozhong Hu, Jing Ann Transl Med Original Article BACKGROUND: Myocardial ischemia (MI) often causes angina, arrhythmia, and cardiac insufficiency, sometimes resulting in death. Ischemia-induced myocardial tissue damage is attributed to the hypoxic damage of myocardial cells producing apoptosis and decreased proliferation. Taurine has been shown to improve MI, but its mechanism is largely unknown. METHODS: In this study, the relationship between taurine and severity of MI in vivo was evaluated by quantifying myocardial infarct areas and metabolic indicators of myocardial damage and measuring taurine levels in cardiac muscle and plasma by high performance liquid chromatography (HPLC). To elucidate how taurine might suppress ischemic injury, we established an in vitro ischemia model with isolated primary rat cardiomyocytes cultured without serum or glucose and under hypoxia. We evaluated the indicators of MI and damage, including lactic dehydrogenase (LDH), creatine kinase (CK), and cardiac troponin I (cTnI). We also examined the levels of taurine transporter (TauT), cysteine dioxygenase (CDO), and cysteine sulfinate decarboxylase (CSD) proteins involved in transport and synthesis of taurine in the myocardium and those of 2 apoptosis-associated proteins, namely, Bcl-2 associated X protein (BAX) and B-cell lymphoma-2 (Bcl-2). RESULTS: Exposure of myocardial cells to ischemia led to the decrease of taurine content, the suppression of cell proliferation, and led to calcium ion overload and apoptosis. Pretreatment with taurine alleviated the ischemic damage, with concomitant elevation of intracellular taurine concentrations. Molecular mechanism analysis showed that pretreatment with taurine upregulated the TauT, CDO, and CSD, 2 rate-limiting enzymes involved in taurine synthesis. These effects facilitated both taurine transport into cells and taurine synthesis, leading to taurine accumulation. In addition, apoptosis inhibition by taurine appeared to be mediated by upregulated Bcl-2 and downregulated BAX, as well as inhibition of calcium overload by suppression of calcium binding protein. CONCLUSIONS: We demonstrated that TauT is critical for the attenuation of myocardial ischemic damage by taurine, facilitating taurine absorption and synthesis. These findings provided new insights and a theoretical foundation for future studies examining taurine as a potential treatment for MI. AME Publishing Company 2021-06 /pmc/articles/PMC8267305/ /pubmed/34277784 http://dx.doi.org/10.21037/atm-21-2481 Text en 2021 Annals of Translational Medicine. All rights reserved. https://creativecommons.org/licenses/by-nc-nd/4.0/Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) .
spellingShingle Original Article
Ren, Fengyun
Liu, Xing
Liu, Xiaoxue
Cao, Yanli
Liu, Lantao
Li, Xingjiang
Wu, Yingjun
Du, Shudi
Tian, Guozhong
Hu, Jing
In vitro and in vivo study on prevention of myocardial ischemic injury by taurine
title In vitro and in vivo study on prevention of myocardial ischemic injury by taurine
title_full In vitro and in vivo study on prevention of myocardial ischemic injury by taurine
title_fullStr In vitro and in vivo study on prevention of myocardial ischemic injury by taurine
title_full_unstemmed In vitro and in vivo study on prevention of myocardial ischemic injury by taurine
title_short In vitro and in vivo study on prevention of myocardial ischemic injury by taurine
title_sort in vitro and in vivo study on prevention of myocardial ischemic injury by taurine
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8267305/
https://www.ncbi.nlm.nih.gov/pubmed/34277784
http://dx.doi.org/10.21037/atm-21-2481
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