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Protection of melatonin against acidosis‐induced neuronal injuries

Acidosis, a common feature of cerebral ischaemia and hypoxia, plays a key role in these pathological processes by aggravating the ischaemic and hypoxic injuries. To explore the mechanisms, in this research, we cultured primary neurons in an acidic environment (potential of hydrogen [pH]6.2, 24 hours...

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Autores principales: Shi, Yan, Cai, Er‐Li, Yang, Can, Ye, Chao‐Yuan, Zeng, Peng, Wang, Xiao‐Ming, Fang, Ying‐Yan, Cheng, Zhi‐Kang, Wang, Qun, Cao, Fu‐Yuan, Zhou, Xin‐Wen, Tian, Qing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7299701/
https://www.ncbi.nlm.nih.gov/pubmed/32364678
http://dx.doi.org/10.1111/jcmm.15351
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author Shi, Yan
Cai, Er‐Li
Yang, Can
Ye, Chao‐Yuan
Zeng, Peng
Wang, Xiao‐Ming
Fang, Ying‐Yan
Cheng, Zhi‐Kang
Wang, Qun
Cao, Fu‐Yuan
Zhou, Xin‐Wen
Tian, Qing
author_facet Shi, Yan
Cai, Er‐Li
Yang, Can
Ye, Chao‐Yuan
Zeng, Peng
Wang, Xiao‐Ming
Fang, Ying‐Yan
Cheng, Zhi‐Kang
Wang, Qun
Cao, Fu‐Yuan
Zhou, Xin‐Wen
Tian, Qing
author_sort Shi, Yan
collection PubMed
description Acidosis, a common feature of cerebral ischaemia and hypoxia, plays a key role in these pathological processes by aggravating the ischaemic and hypoxic injuries. To explore the mechanisms, in this research, we cultured primary neurons in an acidic environment (potential of hydrogen [pH]6.2, 24 hours) to mimic the acidosis. By proteomic analysis, 69 differentially expressed proteins in the acidic neurons were found, mainly related to stress and cell death, synaptic plasticity and gene transcription. And, the acidotic neurons developed obvious alterations including increased neuronal death, reduced dendritic length and complexity, reduced synaptic proteins, tau hyperphosphorylation, endoplasmic reticulum (ER) stress activation, abnormal lysosome‐related signals, imbalanced oxidative stress/anti‐oxidative stress and decreased Golgi matrix proteins. Then, melatonin (1 × 10(−4) mol/L) was used to pre‐treat the cultured primary neurons before acidic treatment (pH6.2). The results showed that melatonin partially reversed the acidosis‐induced neuronal death, abnormal dendritic complexity, reductions of synaptic proteins, tau hyperphosphorylation and imbalance of kinase/phosphatase. In addition, acidosis related the activations of glycogen synthase kinase‐3β and nuclear factor‐κB signals, ER stress and Golgi stress, and the abnormal autophagy‐lysosome signals were completely reversed by melatonin. These data indicate that melatonin is beneficial for neurons against acidosis‐induced injuries.
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spelling pubmed-72997012020-06-18 Protection of melatonin against acidosis‐induced neuronal injuries Shi, Yan Cai, Er‐Li Yang, Can Ye, Chao‐Yuan Zeng, Peng Wang, Xiao‐Ming Fang, Ying‐Yan Cheng, Zhi‐Kang Wang, Qun Cao, Fu‐Yuan Zhou, Xin‐Wen Tian, Qing J Cell Mol Med Original Articles Acidosis, a common feature of cerebral ischaemia and hypoxia, plays a key role in these pathological processes by aggravating the ischaemic and hypoxic injuries. To explore the mechanisms, in this research, we cultured primary neurons in an acidic environment (potential of hydrogen [pH]6.2, 24 hours) to mimic the acidosis. By proteomic analysis, 69 differentially expressed proteins in the acidic neurons were found, mainly related to stress and cell death, synaptic plasticity and gene transcription. And, the acidotic neurons developed obvious alterations including increased neuronal death, reduced dendritic length and complexity, reduced synaptic proteins, tau hyperphosphorylation, endoplasmic reticulum (ER) stress activation, abnormal lysosome‐related signals, imbalanced oxidative stress/anti‐oxidative stress and decreased Golgi matrix proteins. Then, melatonin (1 × 10(−4) mol/L) was used to pre‐treat the cultured primary neurons before acidic treatment (pH6.2). The results showed that melatonin partially reversed the acidosis‐induced neuronal death, abnormal dendritic complexity, reductions of synaptic proteins, tau hyperphosphorylation and imbalance of kinase/phosphatase. In addition, acidosis related the activations of glycogen synthase kinase‐3β and nuclear factor‐κB signals, ER stress and Golgi stress, and the abnormal autophagy‐lysosome signals were completely reversed by melatonin. These data indicate that melatonin is beneficial for neurons against acidosis‐induced injuries. John Wiley and Sons Inc. 2020-05-04 2020-06 /pmc/articles/PMC7299701/ /pubmed/32364678 http://dx.doi.org/10.1111/jcmm.15351 Text en © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd This is an open access article under the terms of the http://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
Shi, Yan
Cai, Er‐Li
Yang, Can
Ye, Chao‐Yuan
Zeng, Peng
Wang, Xiao‐Ming
Fang, Ying‐Yan
Cheng, Zhi‐Kang
Wang, Qun
Cao, Fu‐Yuan
Zhou, Xin‐Wen
Tian, Qing
Protection of melatonin against acidosis‐induced neuronal injuries
title Protection of melatonin against acidosis‐induced neuronal injuries
title_full Protection of melatonin against acidosis‐induced neuronal injuries
title_fullStr Protection of melatonin against acidosis‐induced neuronal injuries
title_full_unstemmed Protection of melatonin against acidosis‐induced neuronal injuries
title_short Protection of melatonin against acidosis‐induced neuronal injuries
title_sort protection of melatonin against acidosis‐induced neuronal injuries
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7299701/
https://www.ncbi.nlm.nih.gov/pubmed/32364678
http://dx.doi.org/10.1111/jcmm.15351
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