G-1 exhibit antidepressant effect, increase of hippocampal ERs expression and improve hippocampal redox status in aged female rats.


Journal

Behavioural brain research
ISSN: 1872-7549
Titre abrégé: Behav Brain Res
Pays: Netherlands
ID NLM: 8004872

Informations de publication

Date de publication:
01 02 2019
Historique:
received: 22 04 2018
revised: 09 07 2018
accepted: 20 07 2018
pubmed: 25 7 2018
medline: 4 4 2019
entrez: 25 7 2018
Statut: ppublish

Résumé

Postmenopausal depression has been shown to be related to the reduction of ovarian hormones produced as a woman transitions from a menopausal to a post-menopausal stage. What remains to be known is which type of estrogen receptor plays a key role in estrogen neuroprotection, a process that may be mediated by potentiating brain mitochondrial function and inhibiting mitochondria-associated apoptosis. In order to better imitate the condition of postmenopause, we conducted our research on aged female rats. Plasma estrogen levels declined significantly in ovariectomized rats and 16-month-old female rats, while anxiety and depression-like behavior increase. Moreover, ERα, ERβ, GPER, Bcl2 and UCP2 expression decreased significantly in hippocampus in female rats following ovariectomy. In our study, the anxiety and depression-like behavior in aged female rats were significantly relieved after the treatment of G-1, the GPER agonist. Furthermore, G-1 could reverse the reduction of ERα, ERβ, GPER, Bcl2 and UCP2 expression within the hippocampus. Mitochondrial JC-1 staining indicated that mitochondrial membrane potential increased after G-1 treatment. In addition, total antioxidant capacity (TAC) and superoxide dismutase activity (SOD) were found to be elevated in aged female rats following G-1 treatment. Taken together, estrogen receptors, especially GPER, may activate anti-apoptotic signaling and accelerate mitochondrial function. Therefore, GPER could be the potential therapeutic target for estrogen deficiency-related affective disorders.

Identifiants

pubmed: 30041006
pii: S0166-4328(18)30575-8
doi: 10.1016/j.bbr.2018.07.017
pii:
doi:

Substances chimiques

1-(4-(6-bromobenzo(1,3)dioxol-5-yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta(c)quinolin-8-yl)ethanone 0
Cyclopentanes 0
Estrogens 0
Quinolines 0
Receptors, Estrogen 0
Superoxide Dismutase EC 1.15.1.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

845-852

Informations de copyright

Copyright © 2018 Elsevier B.V. All rights reserved.

Auteurs

Jing Wang (J)

Department of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, China.

Rui Yu (R)

Department of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, China.

Qiu-Qin Han (QQ)

Department of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, China.

Hui-Jie Huang (HJ)

Department of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, China.

Ya-Lin Wang (YL)

Department of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, China.

Hao-Yuan Li (HY)

Department of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, China; Experimental Teaching Center, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai 200032, China.

Hui-Mei Wang (HM)

Department of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, China; Experimental Teaching Center, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai 200032, China.

Xiao-Rong Chen (XR)

Department of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, China; Experimental Teaching Center, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai 200032, China.

Shu-Lan Ma (SL)

Experimental Teaching Center, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai 200032, China. Electronic address: slma@fudan.edu.cn.

Jin Yu (J)

Department of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, China. Electronic address: yujin@shmu.edu.cn.

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Classifications MeSH