Cargando…
High-concentration hydrogen protects mouse heart against ischemia/reperfusion injury through activation of thePI3K/Akt1 pathway
The study investigated the role of Akt1 through the cardioprotection of high-concentration hydrogen (HCH). C57BL/6 mice were randomly divided into the following groups: sham, I/R, I/R + HCH, I/R + HCH + LY294002 (PI3K inhibitor), I/R + HCH + wortmannin (PI3K inhibitor), I/R + LY294002, and I/R + wor...
Autores principales: | , , , , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2017
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5665927/ https://www.ncbi.nlm.nih.gov/pubmed/29093541 http://dx.doi.org/10.1038/s41598-017-14072-x |
_version_ | 1783275212198903808 |
---|---|
author | Chen, Ouyang Cao, Zhiyong Li, He Ye, Zhouheng Zhang, Rongjia Zhang, Ning Huang, Junlong Zhang, Ting Wang, Liping Han, Ling Liu, Wenwu Sun, Xuejun |
author_facet | Chen, Ouyang Cao, Zhiyong Li, He Ye, Zhouheng Zhang, Rongjia Zhang, Ning Huang, Junlong Zhang, Ting Wang, Liping Han, Ling Liu, Wenwu Sun, Xuejun |
author_sort | Chen, Ouyang |
collection | PubMed |
description | The study investigated the role of Akt1 through the cardioprotection of high-concentration hydrogen (HCH). C57BL/6 mice were randomly divided into the following groups: sham, I/R, I/R + HCH, I/R + HCH + LY294002 (PI3K inhibitor), I/R + HCH + wortmannin (PI3K inhibitor), I/R + LY294002, and I/R + wortmannin. After 45 min of ischemia, HCH (67% H(2) and 33% O(2)) was administered to mice during a 90-min reperfusion. To investigate the role of Akt1 in the protective effects of HCH, mice were divided into the following groups: I/R + A-674563 (Akt1 selective inhibitor), I/R + HCH + A-674563, I/R + CCT128930 (Akt2 selective inhibitor), and I/R + HCH + CCT128930. After a 4-h reperfusion, serum biochemistry, histological, western blotting, and immunohistochemical analyses were performed to evaluate the role of the PI3K-Akt1 pathway in the protection of HCH. In vitro, 75% hydrogen was administered to cardiomyocytes during 4 h of reoxygenation after 3-h hypoxia. Several analyses were performed to evaluate the role of the Akt1 in the protective effects of hydrogen. HCH resulted in the phosphorylation of Akt1 but not Akt2, and Akt1 inhibition markedly abolished HCH-induced cardioprotection. Our findings reveal that HCH may exert cardioprotective effects through a PI3K-Akt1-dependent mechanism. |
format | Online Article Text |
id | pubmed-5665927 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-56659272017-11-08 High-concentration hydrogen protects mouse heart against ischemia/reperfusion injury through activation of thePI3K/Akt1 pathway Chen, Ouyang Cao, Zhiyong Li, He Ye, Zhouheng Zhang, Rongjia Zhang, Ning Huang, Junlong Zhang, Ting Wang, Liping Han, Ling Liu, Wenwu Sun, Xuejun Sci Rep Article The study investigated the role of Akt1 through the cardioprotection of high-concentration hydrogen (HCH). C57BL/6 mice were randomly divided into the following groups: sham, I/R, I/R + HCH, I/R + HCH + LY294002 (PI3K inhibitor), I/R + HCH + wortmannin (PI3K inhibitor), I/R + LY294002, and I/R + wortmannin. After 45 min of ischemia, HCH (67% H(2) and 33% O(2)) was administered to mice during a 90-min reperfusion. To investigate the role of Akt1 in the protective effects of HCH, mice were divided into the following groups: I/R + A-674563 (Akt1 selective inhibitor), I/R + HCH + A-674563, I/R + CCT128930 (Akt2 selective inhibitor), and I/R + HCH + CCT128930. After a 4-h reperfusion, serum biochemistry, histological, western blotting, and immunohistochemical analyses were performed to evaluate the role of the PI3K-Akt1 pathway in the protection of HCH. In vitro, 75% hydrogen was administered to cardiomyocytes during 4 h of reoxygenation after 3-h hypoxia. Several analyses were performed to evaluate the role of the Akt1 in the protective effects of hydrogen. HCH resulted in the phosphorylation of Akt1 but not Akt2, and Akt1 inhibition markedly abolished HCH-induced cardioprotection. Our findings reveal that HCH may exert cardioprotective effects through a PI3K-Akt1-dependent mechanism. Nature Publishing Group UK 2017-11-01 /pmc/articles/PMC5665927/ /pubmed/29093541 http://dx.doi.org/10.1038/s41598-017-14072-x Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Chen, Ouyang Cao, Zhiyong Li, He Ye, Zhouheng Zhang, Rongjia Zhang, Ning Huang, Junlong Zhang, Ting Wang, Liping Han, Ling Liu, Wenwu Sun, Xuejun High-concentration hydrogen protects mouse heart against ischemia/reperfusion injury through activation of thePI3K/Akt1 pathway |
title | High-concentration hydrogen protects mouse heart against ischemia/reperfusion injury through activation of thePI3K/Akt1 pathway |
title_full | High-concentration hydrogen protects mouse heart against ischemia/reperfusion injury through activation of thePI3K/Akt1 pathway |
title_fullStr | High-concentration hydrogen protects mouse heart against ischemia/reperfusion injury through activation of thePI3K/Akt1 pathway |
title_full_unstemmed | High-concentration hydrogen protects mouse heart against ischemia/reperfusion injury through activation of thePI3K/Akt1 pathway |
title_short | High-concentration hydrogen protects mouse heart against ischemia/reperfusion injury through activation of thePI3K/Akt1 pathway |
title_sort | high-concentration hydrogen protects mouse heart against ischemia/reperfusion injury through activation of thepi3k/akt1 pathway |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5665927/ https://www.ncbi.nlm.nih.gov/pubmed/29093541 http://dx.doi.org/10.1038/s41598-017-14072-x |
work_keys_str_mv | AT chenouyang highconcentrationhydrogenprotectsmouseheartagainstischemiareperfusioninjurythroughactivationofthepi3kakt1pathway AT caozhiyong highconcentrationhydrogenprotectsmouseheartagainstischemiareperfusioninjurythroughactivationofthepi3kakt1pathway AT lihe highconcentrationhydrogenprotectsmouseheartagainstischemiareperfusioninjurythroughactivationofthepi3kakt1pathway AT yezhouheng highconcentrationhydrogenprotectsmouseheartagainstischemiareperfusioninjurythroughactivationofthepi3kakt1pathway AT zhangrongjia highconcentrationhydrogenprotectsmouseheartagainstischemiareperfusioninjurythroughactivationofthepi3kakt1pathway AT zhangning highconcentrationhydrogenprotectsmouseheartagainstischemiareperfusioninjurythroughactivationofthepi3kakt1pathway AT huangjunlong highconcentrationhydrogenprotectsmouseheartagainstischemiareperfusioninjurythroughactivationofthepi3kakt1pathway AT zhangting highconcentrationhydrogenprotectsmouseheartagainstischemiareperfusioninjurythroughactivationofthepi3kakt1pathway AT wangliping highconcentrationhydrogenprotectsmouseheartagainstischemiareperfusioninjurythroughactivationofthepi3kakt1pathway AT hanling highconcentrationhydrogenprotectsmouseheartagainstischemiareperfusioninjurythroughactivationofthepi3kakt1pathway AT liuwenwu highconcentrationhydrogenprotectsmouseheartagainstischemiareperfusioninjurythroughactivationofthepi3kakt1pathway AT sunxuejun highconcentrationhydrogenprotectsmouseheartagainstischemiareperfusioninjurythroughactivationofthepi3kakt1pathway |