Cargando…

Hydrogen saline suppresses neuronal cell apoptosis and inhibits the p38 mitogen-activated protein kinase-caspase-3 signaling pathway following cerebral ischemia-reperfusion injury

Cerebral ischemia-reperfusion injury (CIRI) is a serious pathological disease that is associated with a high rate death and disability. Saturated hydrogen (H(2)) saline exhibits brain protective functions through anti-inflammatory, antioxidant and antiapoptotic effects. The present study investigate...

Descripción completa

Detalles Bibliográficos
Autores principales: Li, Da, Ai, Yanqiu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5647063/
https://www.ncbi.nlm.nih.gov/pubmed/28849153
http://dx.doi.org/10.3892/mmr.2017.7294
_version_ 1783272198255935488
author Li, Da
Ai, Yanqiu
author_facet Li, Da
Ai, Yanqiu
author_sort Li, Da
collection PubMed
description Cerebral ischemia-reperfusion injury (CIRI) is a serious pathological disease that is associated with a high rate death and disability. Saturated hydrogen (H(2)) saline exhibits brain protective functions through anti-inflammatory, antioxidant and antiapoptotic effects. The present study investigated the potential treatment effects of H(2) on CIRI. In addition, the potential protective mechanisms of H(2) in the prevention of CIRI were investigated. Adult, male Sprague-Dawley rats (n=60) were randomly divided into the following three groups: Sham-operated group; IR group; and IR + H(2) group (0.6 mmol/l, 0.5 ml/kg/day). Hematoxylin and eosin, and TUNEL staining were performed for histopathological analysis and investigation of apoptosis, respectively. In addition, the protein expression of caspase-3, p38 mitogen-activated protein kinase (MAPK) and phosphorylated-p38 MAPK in the cortex were measured by western blotting analysis. These results demonstrated that H(2) significantly reduced the number of apoptotic cells, and the protein expression of p38 MAPK and caspase-3, compared with the IR group. These effects may be associated with the p38MAPK signaling pathway.
format Online
Article
Text
id pubmed-5647063
institution National Center for Biotechnology Information
language English
publishDate 2017
publisher D.A. Spandidos
record_format MEDLINE/PubMed
spelling pubmed-56470632017-10-24 Hydrogen saline suppresses neuronal cell apoptosis and inhibits the p38 mitogen-activated protein kinase-caspase-3 signaling pathway following cerebral ischemia-reperfusion injury Li, Da Ai, Yanqiu Mol Med Rep Articles Cerebral ischemia-reperfusion injury (CIRI) is a serious pathological disease that is associated with a high rate death and disability. Saturated hydrogen (H(2)) saline exhibits brain protective functions through anti-inflammatory, antioxidant and antiapoptotic effects. The present study investigated the potential treatment effects of H(2) on CIRI. In addition, the potential protective mechanisms of H(2) in the prevention of CIRI were investigated. Adult, male Sprague-Dawley rats (n=60) were randomly divided into the following three groups: Sham-operated group; IR group; and IR + H(2) group (0.6 mmol/l, 0.5 ml/kg/day). Hematoxylin and eosin, and TUNEL staining were performed for histopathological analysis and investigation of apoptosis, respectively. In addition, the protein expression of caspase-3, p38 mitogen-activated protein kinase (MAPK) and phosphorylated-p38 MAPK in the cortex were measured by western blotting analysis. These results demonstrated that H(2) significantly reduced the number of apoptotic cells, and the protein expression of p38 MAPK and caspase-3, compared with the IR group. These effects may be associated with the p38MAPK signaling pathway. D.A. Spandidos 2017-10 2017-08-21 /pmc/articles/PMC5647063/ /pubmed/28849153 http://dx.doi.org/10.3892/mmr.2017.7294 Text en Copyright: © Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Li, Da
Ai, Yanqiu
Hydrogen saline suppresses neuronal cell apoptosis and inhibits the p38 mitogen-activated protein kinase-caspase-3 signaling pathway following cerebral ischemia-reperfusion injury
title Hydrogen saline suppresses neuronal cell apoptosis and inhibits the p38 mitogen-activated protein kinase-caspase-3 signaling pathway following cerebral ischemia-reperfusion injury
title_full Hydrogen saline suppresses neuronal cell apoptosis and inhibits the p38 mitogen-activated protein kinase-caspase-3 signaling pathway following cerebral ischemia-reperfusion injury
title_fullStr Hydrogen saline suppresses neuronal cell apoptosis and inhibits the p38 mitogen-activated protein kinase-caspase-3 signaling pathway following cerebral ischemia-reperfusion injury
title_full_unstemmed Hydrogen saline suppresses neuronal cell apoptosis and inhibits the p38 mitogen-activated protein kinase-caspase-3 signaling pathway following cerebral ischemia-reperfusion injury
title_short Hydrogen saline suppresses neuronal cell apoptosis and inhibits the p38 mitogen-activated protein kinase-caspase-3 signaling pathway following cerebral ischemia-reperfusion injury
title_sort hydrogen saline suppresses neuronal cell apoptosis and inhibits the p38 mitogen-activated protein kinase-caspase-3 signaling pathway following cerebral ischemia-reperfusion injury
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5647063/
https://www.ncbi.nlm.nih.gov/pubmed/28849153
http://dx.doi.org/10.3892/mmr.2017.7294
work_keys_str_mv AT lida hydrogensalinesuppressesneuronalcellapoptosisandinhibitsthep38mitogenactivatedproteinkinasecaspase3signalingpathwayfollowingcerebralischemiareperfusioninjury
AT aiyanqiu hydrogensalinesuppressesneuronalcellapoptosisandinhibitsthep38mitogenactivatedproteinkinasecaspase3signalingpathwayfollowingcerebralischemiareperfusioninjury