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Melatonin inhibits Japanese encephalitis virus replication and neurotoxicity via calcineurin-autophagy pathways
BACKGROUND: Japanese encephalitis virus (JEV) is a mosquito-borne flavivirus that has no specific treatment except for supportive medical care. JEV is a neurotropic virus that affects the nervous system and triggers inflammation in the brain. METHODS: Melatonin is used as a sleep-inducing agent in n...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10629071/ https://www.ncbi.nlm.nih.gov/pubmed/37932682 http://dx.doi.org/10.1186/s12868-023-00832-1 |
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author | Moon, Ji-Hong Hong, Jeong-Min Seol, Jae-Won Park, Byung-Yong Eo, Seong Kug Park, Sang-Youel |
author_facet | Moon, Ji-Hong Hong, Jeong-Min Seol, Jae-Won Park, Byung-Yong Eo, Seong Kug Park, Sang-Youel |
author_sort | Moon, Ji-Hong |
collection | PubMed |
description | BACKGROUND: Japanese encephalitis virus (JEV) is a mosquito-borne flavivirus that has no specific treatment except for supportive medical care. JEV is a neurotropic virus that affects the nervous system and triggers inflammation in the brain. METHODS: Melatonin is used as a sleep-inducing agent in neurophysiology and may serve as a protective agent against neurological and neurodegenerative diseases. Herein, we investigated the effects of melatonin and the critical roles of the serine/threonine protein phosphatase calcineurin during JEV infection in SK-N-SH neuroblastoma cells. RESULTS: Melatonin treatment decreased JEV replication and JEV-mediated neurotoxicity. Calcineurin activity was increased by JEV infection and inhibited by melatonin treatment. Through calcineurin regulation, melatonin decreased the JEV-mediated neuroinflammatory response and attenuated JEV-induced autophagy. CONCLUSIONS: Calcineurin inactivation has a protective effect in JEV-infected neuronal cells, and melatonin is a novel resource for the development of anti-JEV agents. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12868-023-00832-1. |
format | Online Article Text |
id | pubmed-10629071 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-106290712023-11-08 Melatonin inhibits Japanese encephalitis virus replication and neurotoxicity via calcineurin-autophagy pathways Moon, Ji-Hong Hong, Jeong-Min Seol, Jae-Won Park, Byung-Yong Eo, Seong Kug Park, Sang-Youel BMC Neurosci Research BACKGROUND: Japanese encephalitis virus (JEV) is a mosquito-borne flavivirus that has no specific treatment except for supportive medical care. JEV is a neurotropic virus that affects the nervous system and triggers inflammation in the brain. METHODS: Melatonin is used as a sleep-inducing agent in neurophysiology and may serve as a protective agent against neurological and neurodegenerative diseases. Herein, we investigated the effects of melatonin and the critical roles of the serine/threonine protein phosphatase calcineurin during JEV infection in SK-N-SH neuroblastoma cells. RESULTS: Melatonin treatment decreased JEV replication and JEV-mediated neurotoxicity. Calcineurin activity was increased by JEV infection and inhibited by melatonin treatment. Through calcineurin regulation, melatonin decreased the JEV-mediated neuroinflammatory response and attenuated JEV-induced autophagy. CONCLUSIONS: Calcineurin inactivation has a protective effect in JEV-infected neuronal cells, and melatonin is a novel resource for the development of anti-JEV agents. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12868-023-00832-1. BioMed Central 2023-11-06 /pmc/articles/PMC10629071/ /pubmed/37932682 http://dx.doi.org/10.1186/s12868-023-00832-1 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Moon, Ji-Hong Hong, Jeong-Min Seol, Jae-Won Park, Byung-Yong Eo, Seong Kug Park, Sang-Youel Melatonin inhibits Japanese encephalitis virus replication and neurotoxicity via calcineurin-autophagy pathways |
title | Melatonin inhibits Japanese encephalitis virus replication and neurotoxicity via calcineurin-autophagy pathways |
title_full | Melatonin inhibits Japanese encephalitis virus replication and neurotoxicity via calcineurin-autophagy pathways |
title_fullStr | Melatonin inhibits Japanese encephalitis virus replication and neurotoxicity via calcineurin-autophagy pathways |
title_full_unstemmed | Melatonin inhibits Japanese encephalitis virus replication and neurotoxicity via calcineurin-autophagy pathways |
title_short | Melatonin inhibits Japanese encephalitis virus replication and neurotoxicity via calcineurin-autophagy pathways |
title_sort | melatonin inhibits japanese encephalitis virus replication and neurotoxicity via calcineurin-autophagy pathways |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10629071/ https://www.ncbi.nlm.nih.gov/pubmed/37932682 http://dx.doi.org/10.1186/s12868-023-00832-1 |
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