Abstract
New glucagon-like peptide-1 (GLP-1) analogues developed in recent years have a long half-life and offer further prospects for clinical application. At present, the neuroprotection of GLP-1 analogues in Alzheimer's disease (AD) has just begun to be explored. To investigate how glucagon-like peptide-1 (liraglutide) plays a protective role in AD by regulating tau activation and BACE1 expression. Human neuroblastoma cell line SH-SY5Y cells were cultured in vitro and pretreated with different concentrations of liraglutide, and then treated with different concentrations of okadaic acid (OA) in order to observe the apoptosis of the SH-SY5Y cells. After liraglutide treatment, the apoptosis of neurons in AD rats was detected using flow cytometry, and tau activation and β-site APP cleaving enzyme 1 (BACE1) expression were detected using western blot. Different concentrations of OA were able to induce apoptosis of SH-SY5Y cells in a dose-dependent manner. Different concentrations of liraglutide were used to pretreat SH-SY5Y cells, which were able to protect the SH-SY5Y cells from apoptosis induced by OA. Okadaic acid significantly increased tau activation and BACE1 expression in the SH-SY5Y cells, which was blocked with liraglutide pretreatment. The results of a water maze experiment showed that liraglutide had significant protective effects on memory and cognitive ability in AD rats induced with OA, inhibited apoptosis of neural cells in AD rats, and inhibited tau activation and BACE1 expression of neural cells in AD rats induced with OA. Liraglutide has a protective effect on AD in vivo and in vitro, which may be mediated by preventing neuronal apoptosis and inhibiting the activation of tau and the expression of BACE1.
Highlights
Alzheimer’s disease (AD) is a primary degenerative disease of the central nervous system which seriously affects quality of life
Okadaic acid significantly increased tau activation and BACE1 expression in the SH-SY5Y cells, which was blocked with liraglutide pretreatment
The results of a water maze experiment showed that liraglutide had significant protective effects on memory and cognitive ability in AD rats induced with okadaic acid (OA), inhibited apoptosis of neural cells in AD rats, and inhibited tau activation and BACE1 expression of neural cells in AD rats induced with OA
Summary
Alzheimer’s disease (AD) is a primary degenerative disease of the central nervous system which seriously affects quality of life. Glucagonlike peptide-1 (GLP-1) has been found to have neurotrophic and protective effects.[4,5]. The GLP-1 receptor activation can be used to treat type 2 diabetes mellitus.[6]. Because AD and type 2 diabetes mellitus share a common pathogenesis, the use of GLP-1 receptor activation in the treatment of AD has attracted the attention of scholars around the world.[7]. The new GLP-1 analogues developed in recent years have a long half-life and offer more prospects for clinical application. The neuroprotection of GLP-1 analogues on AD has just begun to be explored. New glucagon-like peptide-1 (GLP-1) analogues developed in recent years have a long halflife and offer further prospects for clinical application. The neuroprotection of GLP-1 analogues in Alzheimer’s disease (AD) has just begun to be explored
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