IMR Press / JIN / Volume 20 / Issue 1 / DOI: 10.31083/j.jin.2021.01.242
Open Access Original Research
Geniposide protection against Aβ1-42 toxicity correlates with mTOR inhibition and enhancement of autophagy
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1 Key Laboratory of Cellular Physiology, Shanxi Medical University, Taiyuan, 030606 Shanxi, P. R. China
2 Neurology Department, Shanxi Cardiovascular Hospital, Taiyuan, 030001 Shanxi, P. R. China
3 Chemistry department, Shanxi Medical University, Taiyuan, 030606 Shanxi, P. R. China
4 Neurology Department, Second hospital, Shanxi Medical University, Taiyuan, 030606 Shanxi, P. R. China
5 Pathology department, Shanxi Medical University, Taiyuan, 030606 Shanxi, P. R. China
*Correspondence: lilinsubmission@163.com (Lin Li)
These authors contributed equally.
J. Integr. Neurosci. 2021, 20(1), 67–75; https://doi.org/10.31083/j.jin.2021.01.242
Submitted: 13 August 2020 | Revised: 13 January 2021 | Accepted: 27 January 2021 | Published: 30 March 2021
Copyright: © 2021 The Authors. Published by IMR Press.
This is an open access article under the CC BY 4.0 license (https://creativecommons.org/licenses/by/4.0/).
Abstract

Overactivation of the PI3-K/Akt/mTOR signaling pathway and inhibition of autophagy in the brain are involved in Alzheimer’s disease. The present paper’s goal was to explore the potential mechanisms of geniposide to protect against Alzheimer’s disease. We treated the human neuroblastoma SH-SY5Y cell line with Aβ1-42 as an Alzheimer’s disease in vitro model to explore the potential mechanisms of geniposide to protect against Alzheimer’s disease. Further, SH-SY5Y cells damaged by Aβ1-42 were treated with geniposide. Akt/mTOR-related proteins and autophagy-associated proteins were measured to reveal the molecular mechanisms by which geniposide protects against Aβ1-42-induced toxicity. Results showed that Akt and mTOR’s geniposide inhibited phosphorylation induced by Aβ1-42, enhanced expression of the LC3II/LC3I ratio, and Atg7 and Beclin1 expression and inhibited expression of p62 induced by Aβ1-42. Our results lead us to hypothesize that inhibition of the Akt/mTOR signaling pathway and autophagy enhancement are fundamental molecular mechanisms for geniposide to protect against Aβ toxicity.

Keywords
Geniposide
PI3K
Akt
mTOR
Autophagy
Aβ
Neurodegeneration
Alzheimer's disease
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