Sevoflurane protects against cerebral ischemia/reperfusion injury via microRNA-30c-5p modulating Homeodomain-interacting protein kinase 1

Sevoflurane (SEV) has been reported to be an effective neuroprotective agent for cerebral ischemia/reperfusion injury (CIRI). However, the precise molecular mechanisms of SEV preconditioning in CIRI remain largely unknown. Therefore, CIRI model was established via Middle Cerebral Artery Occlusion me...

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Autores principales: GuoNing Su, Yan Qu, Gang Li, Min Deng
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Lenguaje:EN
Publicado: Taylor & Francis Group 2021
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Acceso en línea:https://doaj.org/article/08a082d41f86473b8f5901ddd5aed4f7
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spelling oai:doaj.org-article:08a082d41f86473b8f5901ddd5aed4f72021-11-04T15:51:54ZSevoflurane protects against cerebral ischemia/reperfusion injury via microRNA-30c-5p modulating Homeodomain-interacting protein kinase 12165-59792165-598710.1080/21655979.2021.1999551https://doaj.org/article/08a082d41f86473b8f5901ddd5aed4f72021-10-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.1999551https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987Sevoflurane (SEV) has been reported to be an effective neuroprotective agent for cerebral ischemia/reperfusion injury (CIRI). However, the precise molecular mechanisms of SEV preconditioning in CIRI remain largely unknown. Therefore, CIRI model was established via Middle Cerebral Artery Occlusion method. SEV was applied before modeling. After successful modeling, lentivirus was injected into the lateral ventricle of the brain. Neurological impairment score was performed in each group, and histopathologic condition, infarct volume, apoptosis, inflammation, oxidative stress, microRNA (miR)-30c-5p and Homeodomain-interacting protein kinase 1 (HIPK1) were detected. Mouse Hippocampal Neuronal Cell Line HT22 cells were pretreated with SEV, and the in vitro model was stimulated via oxygen-glucose deprivation and reoxygenation. The corresponding plasmids were transfected, and the cell growth was detected, including inflammation and oxidative stress, etc. The targeting of miR-30c-5p with HIPK1 was examined. The results clarified that reduced miR-30c-5p and elevated HIPK1 were manifested in CIRI. SEV could improve CIRI and modulate the miR-30c-5p-HIPK1 axis in vitro and in vivo, and miR-30c-5p could target HIPK1. Depressed miR-30c-5p could eliminate the protection of SEV in vitro and in vivo. Repression of HIPK1 reversed the effect of reduced miR-30c-5p on CIRI. Therefore, it is concluded that SEV is available to depress CIRI via targeting HIPK1 through upregulated miR-30c-5p.GuoNing SuYan QuGang LiMin DengTaylor & Francis Grouparticlecerebral ischemia-reperfusion injurysevofluranemicrorna-30c-5phomeodomain-interacting protein kinase 1BiotechnologyTP248.13-248.65ENBioengineered, Vol 0, Iss 0 (2021)
institution DOAJ
collection DOAJ
language EN
topic cerebral ischemia-reperfusion injury
sevoflurane
microrna-30c-5p
homeodomain-interacting protein kinase 1
Biotechnology
TP248.13-248.65
spellingShingle cerebral ischemia-reperfusion injury
sevoflurane
microrna-30c-5p
homeodomain-interacting protein kinase 1
Biotechnology
TP248.13-248.65
GuoNing Su
Yan Qu
Gang Li
Min Deng
Sevoflurane protects against cerebral ischemia/reperfusion injury via microRNA-30c-5p modulating Homeodomain-interacting protein kinase 1
description Sevoflurane (SEV) has been reported to be an effective neuroprotective agent for cerebral ischemia/reperfusion injury (CIRI). However, the precise molecular mechanisms of SEV preconditioning in CIRI remain largely unknown. Therefore, CIRI model was established via Middle Cerebral Artery Occlusion method. SEV was applied before modeling. After successful modeling, lentivirus was injected into the lateral ventricle of the brain. Neurological impairment score was performed in each group, and histopathologic condition, infarct volume, apoptosis, inflammation, oxidative stress, microRNA (miR)-30c-5p and Homeodomain-interacting protein kinase 1 (HIPK1) were detected. Mouse Hippocampal Neuronal Cell Line HT22 cells were pretreated with SEV, and the in vitro model was stimulated via oxygen-glucose deprivation and reoxygenation. The corresponding plasmids were transfected, and the cell growth was detected, including inflammation and oxidative stress, etc. The targeting of miR-30c-5p with HIPK1 was examined. The results clarified that reduced miR-30c-5p and elevated HIPK1 were manifested in CIRI. SEV could improve CIRI and modulate the miR-30c-5p-HIPK1 axis in vitro and in vivo, and miR-30c-5p could target HIPK1. Depressed miR-30c-5p could eliminate the protection of SEV in vitro and in vivo. Repression of HIPK1 reversed the effect of reduced miR-30c-5p on CIRI. Therefore, it is concluded that SEV is available to depress CIRI via targeting HIPK1 through upregulated miR-30c-5p.
format article
author GuoNing Su
Yan Qu
Gang Li
Min Deng
author_facet GuoNing Su
Yan Qu
Gang Li
Min Deng
author_sort GuoNing Su
title Sevoflurane protects against cerebral ischemia/reperfusion injury via microRNA-30c-5p modulating Homeodomain-interacting protein kinase 1
title_short Sevoflurane protects against cerebral ischemia/reperfusion injury via microRNA-30c-5p modulating Homeodomain-interacting protein kinase 1
title_full Sevoflurane protects against cerebral ischemia/reperfusion injury via microRNA-30c-5p modulating Homeodomain-interacting protein kinase 1
title_fullStr Sevoflurane protects against cerebral ischemia/reperfusion injury via microRNA-30c-5p modulating Homeodomain-interacting protein kinase 1
title_full_unstemmed Sevoflurane protects against cerebral ischemia/reperfusion injury via microRNA-30c-5p modulating Homeodomain-interacting protein kinase 1
title_sort sevoflurane protects against cerebral ischemia/reperfusion injury via microrna-30c-5p modulating homeodomain-interacting protein kinase 1
publisher Taylor & Francis Group
publishDate 2021
url https://doaj.org/article/08a082d41f86473b8f5901ddd5aed4f7
work_keys_str_mv AT guoningsu sevofluraneprotectsagainstcerebralischemiareperfusioninjuryviamicrorna30c5pmodulatinghomeodomaininteractingproteinkinase1
AT yanqu sevofluraneprotectsagainstcerebralischemiareperfusioninjuryviamicrorna30c5pmodulatinghomeodomaininteractingproteinkinase1
AT gangli sevofluraneprotectsagainstcerebralischemiareperfusioninjuryviamicrorna30c5pmodulatinghomeodomaininteractingproteinkinase1
AT mindeng sevofluraneprotectsagainstcerebralischemiareperfusioninjuryviamicrorna30c5pmodulatinghomeodomaininteractingproteinkinase1
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