Cargando…

Dihydromyricetin ameliorates social isolation-induced anxiety by modulating mitochondrial function, antioxidant enzymes, and BDNF

Stress has been implicated in the etiology of neurological and psychological illnesses. Chronic social isolation (SI) is a psychological stressor that provokes neurobehavioral changes associated with psychiatric disorders, including anxiety disorders. Mitochondria dysfunction and oxidative stress ar...

Descripción completa

Detalles Bibliográficos
Autores principales: Al Omran, Alzahra J., Watanabe, Saki, Hong, Ethan C., Skinner, Samantha G., Zhang, Mindy, Zhang, Jifeng, Shao, Xuesi M., Liang, Jing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9755067/
https://www.ncbi.nlm.nih.gov/pubmed/36532369
http://dx.doi.org/10.1016/j.ynstr.2022.100499
_version_ 1784851345881169920
author Al Omran, Alzahra J.
Watanabe, Saki
Hong, Ethan C.
Skinner, Samantha G.
Zhang, Mindy
Zhang, Jifeng
Shao, Xuesi M.
Liang, Jing
author_facet Al Omran, Alzahra J.
Watanabe, Saki
Hong, Ethan C.
Skinner, Samantha G.
Zhang, Mindy
Zhang, Jifeng
Shao, Xuesi M.
Liang, Jing
author_sort Al Omran, Alzahra J.
collection PubMed
description Stress has been implicated in the etiology of neurological and psychological illnesses. Chronic social isolation (SI) is a psychological stressor that provokes neurobehavioral changes associated with psychiatric disorders, including anxiety disorders. Mitochondria dysfunction and oxidative stress are hallmarks of anxiety pathogenesis. Here we demonstrate the effects of SI-induced stress on mitochondrial function, antioxidative enzymes, autophagy, and brain derivative neurotrophic factor (BDNF). SI induced a reduction in electron transport chain subunits C–I, C-II, and C-VI and an increase in hydrogen peroxide. Treatment with dihydromyricetin (DHM), extracted from Ampelopsis grossedentata, counteracted these changes. A dramatic increase in several primary mitochondrial antioxidative enzymes such as superoxide dismutase 2 (SOD2), heme oxygenase-1 (HO-1), peroxiredoxin-3 (PRDX3), and glutathione peroxidase 4 (GPX4) was observed after SI and a repeated episode of SI. Both SI and repeated SI induced a reduction in sequestosome 1 (SQSTM1/p62). However, only repeated SI modulated autophagy primary protein beclin-1 (Bcl-1). In addition, SI and repeated SI modulated the BDNF-TrkB signaling pathway and the phosphorylation of the downstream extracellular signal-regulated MAP kinase1/2 (p-Erk p42 and p-Erk p44) cascade. DHM treatment ameliorated these changes. Collectively, we demonstrated that DHM treatment counteracted the effects of SI and repeated SI on antioxidative enzymes, autophagy, and the BDNF-TrkB signaling pathway. These findings highlight the molecular mechanisms that partially explain the anxiolytic effects of DHM.
format Online
Article
Text
id pubmed-9755067
institution National Center for Biotechnology Information
language English
publishDate 2022
publisher Elsevier
record_format MEDLINE/PubMed
spelling pubmed-97550672022-12-17 Dihydromyricetin ameliorates social isolation-induced anxiety by modulating mitochondrial function, antioxidant enzymes, and BDNF Al Omran, Alzahra J. Watanabe, Saki Hong, Ethan C. Skinner, Samantha G. Zhang, Mindy Zhang, Jifeng Shao, Xuesi M. Liang, Jing Neurobiol Stress Original Research Article Stress has been implicated in the etiology of neurological and psychological illnesses. Chronic social isolation (SI) is a psychological stressor that provokes neurobehavioral changes associated with psychiatric disorders, including anxiety disorders. Mitochondria dysfunction and oxidative stress are hallmarks of anxiety pathogenesis. Here we demonstrate the effects of SI-induced stress on mitochondrial function, antioxidative enzymes, autophagy, and brain derivative neurotrophic factor (BDNF). SI induced a reduction in electron transport chain subunits C–I, C-II, and C-VI and an increase in hydrogen peroxide. Treatment with dihydromyricetin (DHM), extracted from Ampelopsis grossedentata, counteracted these changes. A dramatic increase in several primary mitochondrial antioxidative enzymes such as superoxide dismutase 2 (SOD2), heme oxygenase-1 (HO-1), peroxiredoxin-3 (PRDX3), and glutathione peroxidase 4 (GPX4) was observed after SI and a repeated episode of SI. Both SI and repeated SI induced a reduction in sequestosome 1 (SQSTM1/p62). However, only repeated SI modulated autophagy primary protein beclin-1 (Bcl-1). In addition, SI and repeated SI modulated the BDNF-TrkB signaling pathway and the phosphorylation of the downstream extracellular signal-regulated MAP kinase1/2 (p-Erk p42 and p-Erk p44) cascade. DHM treatment ameliorated these changes. Collectively, we demonstrated that DHM treatment counteracted the effects of SI and repeated SI on antioxidative enzymes, autophagy, and the BDNF-TrkB signaling pathway. These findings highlight the molecular mechanisms that partially explain the anxiolytic effects of DHM. Elsevier 2022-10-30 /pmc/articles/PMC9755067/ /pubmed/36532369 http://dx.doi.org/10.1016/j.ynstr.2022.100499 Text en © 2022 The Authors https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Original Research Article
Al Omran, Alzahra J.
Watanabe, Saki
Hong, Ethan C.
Skinner, Samantha G.
Zhang, Mindy
Zhang, Jifeng
Shao, Xuesi M.
Liang, Jing
Dihydromyricetin ameliorates social isolation-induced anxiety by modulating mitochondrial function, antioxidant enzymes, and BDNF
title Dihydromyricetin ameliorates social isolation-induced anxiety by modulating mitochondrial function, antioxidant enzymes, and BDNF
title_full Dihydromyricetin ameliorates social isolation-induced anxiety by modulating mitochondrial function, antioxidant enzymes, and BDNF
title_fullStr Dihydromyricetin ameliorates social isolation-induced anxiety by modulating mitochondrial function, antioxidant enzymes, and BDNF
title_full_unstemmed Dihydromyricetin ameliorates social isolation-induced anxiety by modulating mitochondrial function, antioxidant enzymes, and BDNF
title_short Dihydromyricetin ameliorates social isolation-induced anxiety by modulating mitochondrial function, antioxidant enzymes, and BDNF
title_sort dihydromyricetin ameliorates social isolation-induced anxiety by modulating mitochondrial function, antioxidant enzymes, and bdnf
topic Original Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9755067/
https://www.ncbi.nlm.nih.gov/pubmed/36532369
http://dx.doi.org/10.1016/j.ynstr.2022.100499
work_keys_str_mv AT alomranalzahraj dihydromyricetinamelioratessocialisolationinducedanxietybymodulatingmitochondrialfunctionantioxidantenzymesandbdnf
AT watanabesaki dihydromyricetinamelioratessocialisolationinducedanxietybymodulatingmitochondrialfunctionantioxidantenzymesandbdnf
AT hongethanc dihydromyricetinamelioratessocialisolationinducedanxietybymodulatingmitochondrialfunctionantioxidantenzymesandbdnf
AT skinnersamanthag dihydromyricetinamelioratessocialisolationinducedanxietybymodulatingmitochondrialfunctionantioxidantenzymesandbdnf
AT zhangmindy dihydromyricetinamelioratessocialisolationinducedanxietybymodulatingmitochondrialfunctionantioxidantenzymesandbdnf
AT zhangjifeng dihydromyricetinamelioratessocialisolationinducedanxietybymodulatingmitochondrialfunctionantioxidantenzymesandbdnf
AT shaoxuesim dihydromyricetinamelioratessocialisolationinducedanxietybymodulatingmitochondrialfunctionantioxidantenzymesandbdnf
AT liangjing dihydromyricetinamelioratessocialisolationinducedanxietybymodulatingmitochondrialfunctionantioxidantenzymesandbdnf