The antidepressant effects of ɑ-tocopherol are related to activation of autophagy via the AMPK/mTOR pathway

The purpose of the present study was to investigate whether ɑ-tocopherol exhibited neuro-protective effects in chronic unpredictable mild stress (CUMS) mice through the regulation of autophagy. Deficits in behavioural tests, including a sucrose preference test, open field test, forced swim test, and...

Full description

Saved in:
Bibliographic Details
Published inEuropean journal of pharmacology Vol. 833; pp. 1 - 7
Main Authors Huang, Xiaoyan, Wu, Haoran, Jiang, Ruizhi, Sun, Guangda, Shen, Jiali, Ma, Mengling, Ma, Chuanhui, Zhang, Shijia, Huang, Zhiheng, Wu, Qinan, Chen, Gang, Tao, Weiwei
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 15.08.2018
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:The purpose of the present study was to investigate whether ɑ-tocopherol exhibited neuro-protective effects in chronic unpredictable mild stress (CUMS) mice through the regulation of autophagy. Deficits in behavioural tests, including a sucrose preference test, open field test, forced swim test, and tail suspension test, were ameliorated following ɑ-tocopherol administration. To study the potential mechanism, western blots were performed on both prefrontal cortex and hippocampus samples. Similar to the degree of autophagy, the activities of adenosine monophosphate-activated protein kinase (AMPK) and Unci-51 like autophagy activating kinase-1 (ULK1) were decreased after CUMS stimulation. In addition, we also found increased activity of the mammalian target of rapamycin (mTOR), which was significantly affected following administration of ɑ-tocopherol, as well as its three downstream pathways. Taken together, our study found that ɑ-tocopherol might potentially promote autophagy to induce anti-depressive responses in CUMS mice though the AMPK/mTOR pathway.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0014-2999
1879-0712
DOI:10.1016/j.ejphar.2018.05.020