1. Semaglutide-mediated protection against Aβ correlated with enhancement of autophagy and inhibition of apotosis.
- Author
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Chang YF, Zhang D, Hu WM, Liu DX, and Li L
- Subjects
- Alzheimer Disease pathology, Apoptosis physiology, Autophagy physiology, Cell Line, Tumor, Cell Survival drug effects, Cell Survival physiology, Dose-Response Relationship, Drug, Glucagon-Like Peptides therapeutic use, Humans, Neuroprotective Agents pharmacology, Alzheimer Disease metabolism, Amyloid beta-Peptides toxicity, Apoptosis drug effects, Autophagy drug effects, Glucagon-Like Peptides pharmacology, Peptide Fragments toxicity
- Abstract
Background: Semaglutide, a glucagon-like peptide-1 (GLP-1) analogue with an extended half-life of approximately 1 week has being come into clinic trial to treat parkingson's disease but little is known about its effect to prevent against Alzheimer's disease (AD). The goal of the present study was to explore the potential mechanisms of semaglutide to protect against AD., Methods: We treated SH-SY5Y cell line with Aβ
25-35 as an AD model. Further, SH-SY5Y cells damaged by Aβ25-35 were treated by semaglutide. Autophagy-related proteins and apoptosis-related proteins were measured to explore molecular mechanisms for semaglutide to protect against Aβ25-35 ., Results: Semaglutide enhanced autophagy by increasing the expression of LC3II, Atg7, Beclin-1 and P62 which were inhibited by Aβ25-35 . Further we showed that semaglutide inhibited apoptosis by inhibiting the expression of Bax induced by Aβ25-35 and increasing the expression of Bcl2 inhibited by Aβ25-35 ., Conclusion: Our results provide a clue for the hypothesis that autophagy enhancement and apoptosis inhibition may be involved in the effect of semaglutide to protect against Aβ25-35 ., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Ltd. All rights reserved.)- Published
- 2020
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