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Hydrogen sulfide ameliorates subarachnoid hemorrhage-induced neuronal apoptosis via the ROS-MST1 pathway

BACKGROUND: Hydrogen sulfide (H(2)S) has shown a neuroprotective role in several cerebrovascular diseases. This study aimed to explore the underlying mechanisms of H(2)S in early brain injury after subarachnoid hemorrhage (SAH). METHODS: One hundred seventy-seven male Sprague-Dawley rats were employ...

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Autores principales: Shi, Ligen, Lei, Jianwei, Xu, Hangzhe, Zheng, Jingwei, Wang, Yan, Peng, Yucong, Yu, Jun, Zhang, Jianmin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5650280/
https://www.ncbi.nlm.nih.gov/pubmed/29088725
http://dx.doi.org/10.18632/oncotarget.20569
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author Shi, Ligen
Lei, Jianwei
Xu, Hangzhe
Zheng, Jingwei
Wang, Yan
Peng, Yucong
Yu, Jun
Zhang, Jianmin
author_facet Shi, Ligen
Lei, Jianwei
Xu, Hangzhe
Zheng, Jingwei
Wang, Yan
Peng, Yucong
Yu, Jun
Zhang, Jianmin
author_sort Shi, Ligen
collection PubMed
description BACKGROUND: Hydrogen sulfide (H(2)S) has shown a neuroprotective role in several cerebrovascular diseases. This study aimed to explore the underlying mechanisms of H(2)S in early brain injury after subarachnoid hemorrhage (SAH). METHODS: One hundred seventy-seven male Sprague-Dawley rats were employed in this study. Sodium hydrosulfide (NaHS), a donor of H(2)S, was injected intraperitoneally at 60 min after SAH was induced by endovascular perforation. Western blot analysis determined the expression of several proteins of interest, and an immunofluorescence assay was used to examine neuronal apoptosis. RESULTS: Exogenous NaHS markedly improved neurological scores, attenuated brain edema, and ameliorated neuronal apoptosis at 24 h after SAH induction. The underlying mechanisms of H(2)S in ameliorating neuronal apoptosis might be executed through inhibition of the activity of mammalian sterile 20-like kinase 1 (MST1) protein. Western blot analysis demonstrated that exogenous NaHS decreased cleaved MST1 (cl-MST1) while increasing full-length MST1 expression. This anti-apoptotic effect of H(2)S could be reversed by chelerythrine, which could activate MST1 via caspase-dependent cleavage. CONCLUSIONS: Exogenous NaHS, as a donor of H(2)S, could ameliorate early brain injury after SAH by inhibiting neuronal apoptosis by reducing the activity of the MST1 protein.
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spelling pubmed-56502802017-10-30 Hydrogen sulfide ameliorates subarachnoid hemorrhage-induced neuronal apoptosis via the ROS-MST1 pathway Shi, Ligen Lei, Jianwei Xu, Hangzhe Zheng, Jingwei Wang, Yan Peng, Yucong Yu, Jun Zhang, Jianmin Oncotarget Research Paper: Pathology BACKGROUND: Hydrogen sulfide (H(2)S) has shown a neuroprotective role in several cerebrovascular diseases. This study aimed to explore the underlying mechanisms of H(2)S in early brain injury after subarachnoid hemorrhage (SAH). METHODS: One hundred seventy-seven male Sprague-Dawley rats were employed in this study. Sodium hydrosulfide (NaHS), a donor of H(2)S, was injected intraperitoneally at 60 min after SAH was induced by endovascular perforation. Western blot analysis determined the expression of several proteins of interest, and an immunofluorescence assay was used to examine neuronal apoptosis. RESULTS: Exogenous NaHS markedly improved neurological scores, attenuated brain edema, and ameliorated neuronal apoptosis at 24 h after SAH induction. The underlying mechanisms of H(2)S in ameliorating neuronal apoptosis might be executed through inhibition of the activity of mammalian sterile 20-like kinase 1 (MST1) protein. Western blot analysis demonstrated that exogenous NaHS decreased cleaved MST1 (cl-MST1) while increasing full-length MST1 expression. This anti-apoptotic effect of H(2)S could be reversed by chelerythrine, which could activate MST1 via caspase-dependent cleavage. CONCLUSIONS: Exogenous NaHS, as a donor of H(2)S, could ameliorate early brain injury after SAH by inhibiting neuronal apoptosis by reducing the activity of the MST1 protein. Impact Journals LLC 2017-08-28 /pmc/articles/PMC5650280/ /pubmed/29088725 http://dx.doi.org/10.18632/oncotarget.20569 Text en Copyright: © 2017 Shi et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper: Pathology
Shi, Ligen
Lei, Jianwei
Xu, Hangzhe
Zheng, Jingwei
Wang, Yan
Peng, Yucong
Yu, Jun
Zhang, Jianmin
Hydrogen sulfide ameliorates subarachnoid hemorrhage-induced neuronal apoptosis via the ROS-MST1 pathway
title Hydrogen sulfide ameliorates subarachnoid hemorrhage-induced neuronal apoptosis via the ROS-MST1 pathway
title_full Hydrogen sulfide ameliorates subarachnoid hemorrhage-induced neuronal apoptosis via the ROS-MST1 pathway
title_fullStr Hydrogen sulfide ameliorates subarachnoid hemorrhage-induced neuronal apoptosis via the ROS-MST1 pathway
title_full_unstemmed Hydrogen sulfide ameliorates subarachnoid hemorrhage-induced neuronal apoptosis via the ROS-MST1 pathway
title_short Hydrogen sulfide ameliorates subarachnoid hemorrhage-induced neuronal apoptosis via the ROS-MST1 pathway
title_sort hydrogen sulfide ameliorates subarachnoid hemorrhage-induced neuronal apoptosis via the ros-mst1 pathway
topic Research Paper: Pathology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5650280/
https://www.ncbi.nlm.nih.gov/pubmed/29088725
http://dx.doi.org/10.18632/oncotarget.20569
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