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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...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2020
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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. |
format | Online Article Text |
id | pubmed-7299701 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
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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