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10‐Gingerol alleviates hypoxia/reoxygenation‐induced cardiomyocyte injury through inhibition of the Wnt5a/Frizzled‐2 pathway

10‐Gingerol (10‐Gin), an active ingredient extracted from ginger, has been reported to have beneficial effects on the cardiovascular system. However, 10‐Gin has not been proved to offer protection against cardiomyocyte injury induced by hypoxia/reoxygenation (H/R). This study aimed to investigate th...

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Autores principales: Zheng, Bin, Qi, Jiaying, Liu, Panpan, Zhang, Muqing, Zhang, Yuanyuan, Xue, Yucong, Han, Xue, Xu, Shan, Chu, Li
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8269582/
https://www.ncbi.nlm.nih.gov/pubmed/34262748
http://dx.doi.org/10.1002/fsn3.2381
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author Zheng, Bin
Qi, Jiaying
Liu, Panpan
Zhang, Muqing
Zhang, Yuanyuan
Xue, Yucong
Han, Xue
Xu, Shan
Chu, Li
author_facet Zheng, Bin
Qi, Jiaying
Liu, Panpan
Zhang, Muqing
Zhang, Yuanyuan
Xue, Yucong
Han, Xue
Xu, Shan
Chu, Li
author_sort Zheng, Bin
collection PubMed
description 10‐Gingerol (10‐Gin), an active ingredient extracted from ginger, has been reported to have beneficial effects on the cardiovascular system. However, 10‐Gin has not been proved to offer protection against cardiomyocyte injury induced by hypoxia/reoxygenation (H/R). This study aimed to investigate the protective effects of 10‐Gin against H/R‐induced injury and its potential mechanisms in cardiomyocytes. A H/R injury model of H9c2 cardiomyocytes was established using 600 μmol/L CoCl(2) to induce hypoxia in the cells for 24 hr and then reoxygenated for 3 hr. 10‐Gin was pretreated with H9c2 cardiomyocytes for 24 hr to assess its cardiomyocyte protection. Our results showed that 10‐Gin improved the viability of H9c2 cardiomyocytes in the H/R model and decreased the activities of creatine kinase, lactate dehydrogenase, and the generation of reactive oxygen species. By intracellular Ca(2+) ([Ca(2+)](i)) fluorescence, we found that 10‐Gin could significantly reduce the [Ca(2+)](i) concentration. 10‐Gin administration increased the activities of antioxidase and reduced malondialdehyde content and inflammatory cytokine levels. 10‐Gin also reduced the apoptosis levels. Importantly, 10‐Gin administration decreased the gene and protein expressions of Wnt5a and Frizzled‐2. In conclusion, 10‐Gin alleviates H/R‐induced cardiomyocyte injury, which is associated with the antioxidation, anti‐inflammation, antiapoptosis action, and reduction of [Ca(2+)](i) overload by suppressing the Wnt5a/Frizzled‐2 pathway.
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spelling pubmed-82695822021-07-13 10‐Gingerol alleviates hypoxia/reoxygenation‐induced cardiomyocyte injury through inhibition of the Wnt5a/Frizzled‐2 pathway Zheng, Bin Qi, Jiaying Liu, Panpan Zhang, Muqing Zhang, Yuanyuan Xue, Yucong Han, Xue Xu, Shan Chu, Li Food Sci Nutr Original Research 10‐Gingerol (10‐Gin), an active ingredient extracted from ginger, has been reported to have beneficial effects on the cardiovascular system. However, 10‐Gin has not been proved to offer protection against cardiomyocyte injury induced by hypoxia/reoxygenation (H/R). This study aimed to investigate the protective effects of 10‐Gin against H/R‐induced injury and its potential mechanisms in cardiomyocytes. A H/R injury model of H9c2 cardiomyocytes was established using 600 μmol/L CoCl(2) to induce hypoxia in the cells for 24 hr and then reoxygenated for 3 hr. 10‐Gin was pretreated with H9c2 cardiomyocytes for 24 hr to assess its cardiomyocyte protection. Our results showed that 10‐Gin improved the viability of H9c2 cardiomyocytes in the H/R model and decreased the activities of creatine kinase, lactate dehydrogenase, and the generation of reactive oxygen species. By intracellular Ca(2+) ([Ca(2+)](i)) fluorescence, we found that 10‐Gin could significantly reduce the [Ca(2+)](i) concentration. 10‐Gin administration increased the activities of antioxidase and reduced malondialdehyde content and inflammatory cytokine levels. 10‐Gin also reduced the apoptosis levels. Importantly, 10‐Gin administration decreased the gene and protein expressions of Wnt5a and Frizzled‐2. In conclusion, 10‐Gin alleviates H/R‐induced cardiomyocyte injury, which is associated with the antioxidation, anti‐inflammation, antiapoptosis action, and reduction of [Ca(2+)](i) overload by suppressing the Wnt5a/Frizzled‐2 pathway. John Wiley and Sons Inc. 2021-06-05 /pmc/articles/PMC8269582/ /pubmed/34262748 http://dx.doi.org/10.1002/fsn3.2381 Text en © 2021 The Authors. Food Science & Nutrition published by Wiley Periodicals LLC. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Research
Zheng, Bin
Qi, Jiaying
Liu, Panpan
Zhang, Muqing
Zhang, Yuanyuan
Xue, Yucong
Han, Xue
Xu, Shan
Chu, Li
10‐Gingerol alleviates hypoxia/reoxygenation‐induced cardiomyocyte injury through inhibition of the Wnt5a/Frizzled‐2 pathway
title 10‐Gingerol alleviates hypoxia/reoxygenation‐induced cardiomyocyte injury through inhibition of the Wnt5a/Frizzled‐2 pathway
title_full 10‐Gingerol alleviates hypoxia/reoxygenation‐induced cardiomyocyte injury through inhibition of the Wnt5a/Frizzled‐2 pathway
title_fullStr 10‐Gingerol alleviates hypoxia/reoxygenation‐induced cardiomyocyte injury through inhibition of the Wnt5a/Frizzled‐2 pathway
title_full_unstemmed 10‐Gingerol alleviates hypoxia/reoxygenation‐induced cardiomyocyte injury through inhibition of the Wnt5a/Frizzled‐2 pathway
title_short 10‐Gingerol alleviates hypoxia/reoxygenation‐induced cardiomyocyte injury through inhibition of the Wnt5a/Frizzled‐2 pathway
title_sort 10‐gingerol alleviates hypoxia/reoxygenation‐induced cardiomyocyte injury through inhibition of the wnt5a/frizzled‐2 pathway
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8269582/
https://www.ncbi.nlm.nih.gov/pubmed/34262748
http://dx.doi.org/10.1002/fsn3.2381
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