Melatonin protects against ovarian damage by inhibiting autophagy in granulosa cells in rats
Autor(a) principal: | |
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Data de Publicação: | 2022 |
Outros Autores: | , , , , |
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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oai:revistas.usp.br:article/213568 |
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Clinics |
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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 |
_version_ |
1800222766990884864 |