Melatonin protects against ovarian damage by inhibiting autophagy in granulosa cells in rats

Detalhes bibliográficos
Autor(a) principal: Liu, Yan
Data de Publicação: 2022
Outros Autores: Zhu, Xiaohe, Wu, Chunli, Lang, Yan, Zhao, Wenjie, Li, Yanmin
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Clinics
Texto Completo: https://www.revistas.usp.br/clinics/article/view/213568
Resumo: Objectives: This study sought to further verify the protective mechanism of Melatonin (MT) against ovarian damage through animal model experiments and to lay a theoretical and experimental foundation for exploring new approaches for ovarian damage treatment. Method: The wet weight and ovarian index of rat ovaries were weighted, and the morphology of ovarian tissues and the number of follicles in the pathological sections of collected ovarian tissues were recorded. And the serum sex hormone levels, the key proteins of the autophagy pathway (PI3K, AKT, mTOR, LC3II, LC3I, and Agt5) in rat ovarian tissues, as well as the viability and mortality of ovarian granulosa cells in each group were measured by ELISA, western blotting, CCK8 kit and LDH kit, respectively. Results: The results showed that MT increased ovarian weight and improved the ovarian index in ovarian damage rats. Also, MT could improve autophagy-induced ovarian tissue injury, increase the number of primordial follicles, primary follicles, and sinus follicles, and decrease the number of atretic follicles. Furthermore, MT upregulated serum AMH, INH-B, and E2 levels downregulated serum FSH and LH levels in ovarian damage rats and activated the PI3K/AKT/mTOR signaling pathway. Besides, MT inhibited autophagic apoptosis of ovarian granulosa cells and repressed the expression of key proteins in the autophagic pathway and reduced the expression levels of Agt5 and LC3II/I. Conclusions: MT inhibits granulosa cell autophagy by activating the PI3K/Akt/mTOR signaling pathway, thereby exerting a protective effect against ovarian damage.
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spelling Melatonin protects against ovarian damage by inhibiting autophagy in granulosa cells in ratsAutophagyEffectMelatoninOvarian Granulosa CellsOvarian damageObjectives: This study sought to further verify the protective mechanism of Melatonin (MT) against ovarian damage through animal model experiments and to lay a theoretical and experimental foundation for exploring new approaches for ovarian damage treatment. Method: The wet weight and ovarian index of rat ovaries were weighted, and the morphology of ovarian tissues and the number of follicles in the pathological sections of collected ovarian tissues were recorded. And the serum sex hormone levels, the key proteins of the autophagy pathway (PI3K, AKT, mTOR, LC3II, LC3I, and Agt5) in rat ovarian tissues, as well as the viability and mortality of ovarian granulosa cells in each group were measured by ELISA, western blotting, CCK8 kit and LDH kit, respectively. Results: The results showed that MT increased ovarian weight and improved the ovarian index in ovarian damage rats. Also, MT could improve autophagy-induced ovarian tissue injury, increase the number of primordial follicles, primary follicles, and sinus follicles, and decrease the number of atretic follicles. Furthermore, MT upregulated serum AMH, INH-B, and E2 levels downregulated serum FSH and LH levels in ovarian damage rats and activated the PI3K/AKT/mTOR signaling pathway. Besides, MT inhibited autophagic apoptosis of ovarian granulosa cells and repressed the expression of key proteins in the autophagic pathway and reduced the expression levels of Agt5 and LC3II/I. Conclusions: MT inhibits granulosa cell autophagy by activating the PI3K/Akt/mTOR signaling pathway, thereby exerting a protective effect against ovarian damage.Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo2022-10-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/clinics/article/view/21356810.1016/j.clinsp.2022.100119Clinics; Vol. 77 (2022); 100119Clinics; v. 77 (2022); 100119Clinics; Vol. 77 (2022); 1001191980-53221807-5932reponame:Clinicsinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/clinics/article/view/213568/195645Copyright (c) 2023 Clinicsinfo:eu-repo/semantics/openAccessLiu, YanZhu, XiaoheWu, ChunliLang, YanZhao, WenjieLi, Yanmin2023-07-06T13:04:59Zoai:revistas.usp.br:article/213568Revistahttps://www.revistas.usp.br/clinicsPUBhttps://www.revistas.usp.br/clinics/oai||clinics@hc.fm.usp.br1980-53221807-5932opendoar:2023-07-06T13:04:59Clinics - Universidade de São Paulo (USP)false
dc.title.none.fl_str_mv Melatonin protects against ovarian damage by inhibiting autophagy in granulosa cells in rats
title Melatonin protects against ovarian damage by inhibiting autophagy in granulosa cells in rats
spellingShingle Melatonin protects against ovarian damage by inhibiting autophagy in granulosa cells in rats
Liu, Yan
Autophagy
Effect
Melatonin
Ovarian Granulosa Cells
Ovarian damage
title_short Melatonin protects against ovarian damage by inhibiting autophagy in granulosa cells in rats
title_full Melatonin protects against ovarian damage by inhibiting autophagy in granulosa cells in rats
title_fullStr Melatonin protects against ovarian damage by inhibiting autophagy in granulosa cells in rats
title_full_unstemmed Melatonin protects against ovarian damage by inhibiting autophagy in granulosa cells in rats
title_sort Melatonin protects against ovarian damage by inhibiting autophagy in granulosa cells in rats
author Liu, Yan
author_facet Liu, Yan
Zhu, Xiaohe
Wu, Chunli
Lang, Yan
Zhao, Wenjie
Li, Yanmin
author_role author
author2 Zhu, Xiaohe
Wu, Chunli
Lang, Yan
Zhao, Wenjie
Li, Yanmin
author2_role author
author
author
author
author
dc.contributor.author.fl_str_mv Liu, Yan
Zhu, Xiaohe
Wu, Chunli
Lang, Yan
Zhao, Wenjie
Li, Yanmin
dc.subject.por.fl_str_mv Autophagy
Effect
Melatonin
Ovarian Granulosa Cells
Ovarian damage
topic Autophagy
Effect
Melatonin
Ovarian Granulosa Cells
Ovarian damage
description Objectives: This study sought to further verify the protective mechanism of Melatonin (MT) against ovarian damage through animal model experiments and to lay a theoretical and experimental foundation for exploring new approaches for ovarian damage treatment. Method: The wet weight and ovarian index of rat ovaries were weighted, and the morphology of ovarian tissues and the number of follicles in the pathological sections of collected ovarian tissues were recorded. And the serum sex hormone levels, the key proteins of the autophagy pathway (PI3K, AKT, mTOR, LC3II, LC3I, and Agt5) in rat ovarian tissues, as well as the viability and mortality of ovarian granulosa cells in each group were measured by ELISA, western blotting, CCK8 kit and LDH kit, respectively. Results: The results showed that MT increased ovarian weight and improved the ovarian index in ovarian damage rats. Also, MT could improve autophagy-induced ovarian tissue injury, increase the number of primordial follicles, primary follicles, and sinus follicles, and decrease the number of atretic follicles. Furthermore, MT upregulated serum AMH, INH-B, and E2 levels downregulated serum FSH and LH levels in ovarian damage rats and activated the PI3K/AKT/mTOR signaling pathway. Besides, MT inhibited autophagic apoptosis of ovarian granulosa cells and repressed the expression of key proteins in the autophagic pathway and reduced the expression levels of Agt5 and LC3II/I. Conclusions: MT inhibits granulosa cell autophagy by activating the PI3K/Akt/mTOR signaling pathway, thereby exerting a protective effect against ovarian damage.
publishDate 2022
dc.date.none.fl_str_mv 2022-10-01
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://www.revistas.usp.br/clinics/article/view/213568
10.1016/j.clinsp.2022.100119
url https://www.revistas.usp.br/clinics/article/view/213568
identifier_str_mv 10.1016/j.clinsp.2022.100119
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://www.revistas.usp.br/clinics/article/view/213568/195645
dc.rights.driver.fl_str_mv Copyright (c) 2023 Clinics
info:eu-repo/semantics/openAccess
rights_invalid_str_mv Copyright (c) 2023 Clinics
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
dc.source.none.fl_str_mv Clinics; Vol. 77 (2022); 100119
Clinics; v. 77 (2022); 100119
Clinics; Vol. 77 (2022); 100119
1980-5322
1807-5932
reponame:Clinics
instname:Universidade de São Paulo (USP)
instacron:USP
instname_str Universidade de São Paulo (USP)
instacron_str USP
institution USP
reponame_str Clinics
collection Clinics
repository.name.fl_str_mv Clinics - Universidade de São Paulo (USP)
repository.mail.fl_str_mv ||clinics@hc.fm.usp.br
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