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Isoflurane post‐conditioning contributes to anti‐apoptotic effect after cerebral ischaemia in rats through the ERK5/MEF2D signaling pathway

The mechanisms of brain protection during ischaemic reperfusion injury induced by isoflurane (ISO) post‐conditioning are unclear. Myocyte enhancement factor 2 (MEF2D) has been shown to promote neural survival in a variety of models, in which multiple survival and death signals converge on MEF2D and...

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Autores principales: Zhang, Qingtong, Yin, Jiangwen, Xu, Feng, Zhai, Jingwen, Yin, Jieting, Ge, Mingyue, Zhou, Wenyi, Li, Nian, Qin, Xinlei, Li, Yan, Wang, Sheng
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/PMC8051747/
https://www.ncbi.nlm.nih.gov/pubmed/33621420
http://dx.doi.org/10.1111/jcmm.16282
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author Zhang, Qingtong
Yin, Jiangwen
Xu, Feng
Zhai, Jingwen
Yin, Jieting
Ge, Mingyue
Zhou, Wenyi
Li, Nian
Qin, Xinlei
Li, Yan
Wang, Sheng
author_facet Zhang, Qingtong
Yin, Jiangwen
Xu, Feng
Zhai, Jingwen
Yin, Jieting
Ge, Mingyue
Zhou, Wenyi
Li, Nian
Qin, Xinlei
Li, Yan
Wang, Sheng
author_sort Zhang, Qingtong
collection PubMed
description The mechanisms of brain protection during ischaemic reperfusion injury induced by isoflurane (ISO) post‐conditioning are unclear. Myocyte enhancement factor 2 (MEF2D) has been shown to promote neural survival in a variety of models, in which multiple survival and death signals converge on MEF2D and modulate its activity. Here, we investigated the effect of MEF2D on the neuroprotective effects of ISO post‐conditioning on rats after cerebral ischaemia/reperfusion (I/R) injury. Rats underwent middle cerebral artery occlusion (MCAO) surgery with ischaemia for 90 minutes and reperfusion for 24‐48 hours. After MCAO, neurological status was assessed at 12, 24 and 48 hours by the Modified Neurological Severity Score (mNSS) test. The passive avoidance test (PAT) was used to assess cognition function. Histological and neuropathological evaluations were performed with HE staining and Nissl's staining, respectively. We measured the expression of MEF2D, ERK5, GFAP and caspase‐3 by immunofluorescent staining and Western blotting, and TUNEL staining to assess the severity of apoptosis in hippocampal CA1 area. We found that MEF2D was involved in nerve protection after I/R injury, and post‐treatment of ISO significantly promoted the phosphorylation of ERK5, increased MEF2D transcriptional activity, inhibited the expression of caspase‐3 and played a role of brain protection.
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spelling pubmed-80517472021-04-21 Isoflurane post‐conditioning contributes to anti‐apoptotic effect after cerebral ischaemia in rats through the ERK5/MEF2D signaling pathway Zhang, Qingtong Yin, Jiangwen Xu, Feng Zhai, Jingwen Yin, Jieting Ge, Mingyue Zhou, Wenyi Li, Nian Qin, Xinlei Li, Yan Wang, Sheng J Cell Mol Med Original Articles The mechanisms of brain protection during ischaemic reperfusion injury induced by isoflurane (ISO) post‐conditioning are unclear. Myocyte enhancement factor 2 (MEF2D) has been shown to promote neural survival in a variety of models, in which multiple survival and death signals converge on MEF2D and modulate its activity. Here, we investigated the effect of MEF2D on the neuroprotective effects of ISO post‐conditioning on rats after cerebral ischaemia/reperfusion (I/R) injury. Rats underwent middle cerebral artery occlusion (MCAO) surgery with ischaemia for 90 minutes and reperfusion for 24‐48 hours. After MCAO, neurological status was assessed at 12, 24 and 48 hours by the Modified Neurological Severity Score (mNSS) test. The passive avoidance test (PAT) was used to assess cognition function. Histological and neuropathological evaluations were performed with HE staining and Nissl's staining, respectively. We measured the expression of MEF2D, ERK5, GFAP and caspase‐3 by immunofluorescent staining and Western blotting, and TUNEL staining to assess the severity of apoptosis in hippocampal CA1 area. We found that MEF2D was involved in nerve protection after I/R injury, and post‐treatment of ISO significantly promoted the phosphorylation of ERK5, increased MEF2D transcriptional activity, inhibited the expression of caspase‐3 and played a role of brain protection. John Wiley and Sons Inc. 2021-02-23 2021-04 /pmc/articles/PMC8051747/ /pubmed/33621420 http://dx.doi.org/10.1111/jcmm.16282 Text en © 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. 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 Articles
Zhang, Qingtong
Yin, Jiangwen
Xu, Feng
Zhai, Jingwen
Yin, Jieting
Ge, Mingyue
Zhou, Wenyi
Li, Nian
Qin, Xinlei
Li, Yan
Wang, Sheng
Isoflurane post‐conditioning contributes to anti‐apoptotic effect after cerebral ischaemia in rats through the ERK5/MEF2D signaling pathway
title Isoflurane post‐conditioning contributes to anti‐apoptotic effect after cerebral ischaemia in rats through the ERK5/MEF2D signaling pathway
title_full Isoflurane post‐conditioning contributes to anti‐apoptotic effect after cerebral ischaemia in rats through the ERK5/MEF2D signaling pathway
title_fullStr Isoflurane post‐conditioning contributes to anti‐apoptotic effect after cerebral ischaemia in rats through the ERK5/MEF2D signaling pathway
title_full_unstemmed Isoflurane post‐conditioning contributes to anti‐apoptotic effect after cerebral ischaemia in rats through the ERK5/MEF2D signaling pathway
title_short Isoflurane post‐conditioning contributes to anti‐apoptotic effect after cerebral ischaemia in rats through the ERK5/MEF2D signaling pathway
title_sort isoflurane post‐conditioning contributes to anti‐apoptotic effect after cerebral ischaemia in rats through the erk5/mef2d signaling pathway
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8051747/
https://www.ncbi.nlm.nih.gov/pubmed/33621420
http://dx.doi.org/10.1111/jcmm.16282
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