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The protective effects of liraglutide on AD-like neurodegeneration induced by oxidative stress in human neuroblastoma SH-SY5Y cells.

Chem Biol Interact · 2019

Last updated 2026-05-28

This study tested liraglutide, a drug similar to GLP-1, in lab-grown nerve cells to see if it could protect against damage linked to Alzheimer’s disease. Cells treated with liraglutide showed better survival, less harmful oxidation, and fewer signs of cell death compared to untreated cells. The drug also helped reduce abnormal protein changes tied to Alzheimer’s. The findings suggest liraglutide might have a role in protecting nerve cells, but this was only tested in cells, not people.

AI summary of the abstract below.

JournalChem Biol Interact, 2019
Citations31
Relative citation ratio1.93
NIH percentile72
Molecules liraglutide
Conditions studied Alzheimers

Abstract

Glucagon-like peptide 1 (GLP-1) has neuroprotective properties in Alzheimer's disease (AD). In this study, our aim is to explore the neuroprotective effects of liraglutide, a GLP-1 analogue, on AD-like neurodegeneration induced by HO in human neuroblastoma SH-SY5Y cells. Cytotoxicity was determined by MTT assay and lactate dehydrogenase level was monitored by LDH assay. The level of lipid peroxidation and cell apoptosis rate were measured by malondialdehyde (MDA) assay and Annexin V-FITC/propidium iodide (PI) staining. Western blotting was used to assess the expression of Bcl-2, Bax, caspase-3, tau and the Akt/GSK-3β. Liraglutide pre-treatment enhanced cell viability with reduced cytotoxicity, lipid peroxidationand and apoptosis. In addition, pre-treatment of liraglutide displayed that increased the expression of the pro-survival Bcl-2 and reduced pro-apoptotic Bax with ameliorated the hyperphosphorylation of tau and Akt/GSK-3β signaling pathway in HO stressed SH-SY5Y cells. These finding provided evidences that liraglutide protected the HO induced AD-like neurodegeneration through improving Akt/GSK-3β signaling pathway. These results suggest that liraglutide may have potential values for the treatment for AD.

Verbatim abstract via PubMed 31173752 ↗

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