Neuroprotective effect of sinapic acid in APP/PS1 mouse model and PC12 Cells of Alzheimer's disease via activation of PI3K/Akt/GSK3β signaling pathways.

To explore the neuroprotective effects of Sinapic Acid (SA) in APP/PS1 mouse model and amyloid beta-peptide (Aβ)-induced neuronal cell apoptosis using PC12 cells of Alzheimer's disease. In vivo, the Morris water maze (MWM) test assessed learning and memory abilities, enzyme-linked immunosorbent assay test and immunohistochemistry were conducted to plaque deposition and content of Aβ. Western blotting was performed to p-P13K, P13K, p-Akt, Akt, p-GSK3β and GSK3β expression of the hippocampus in mice, respectively. In vitro, the viability of the cells, the apoptosis of the cells and the level of Bax, Bcl-2, caspase-3, p-P13K, P13K, p-Akt, Akt, p-GSK3β and GSK3β expression of PC12 cells were examined by CCK-8 assay, Hoechst 33342 and Calcein/propidium iodide (PI) staining, flow cytometry and Western blotting, respectively. Our results indicated SA could improve learning and memory abilities and decrease plaque deposition and content of Aβ of the hippocampus in mice. Furthermore, SA increased cell viability and lessened cell apoptosis by increasing the ratio of Bcl-2/Bax, lessening protein levels of Caspase-3 in PC12 cells. SA upregulated the phosphorylation expression level of PI3K/Akt/GSK3β in APP/PS1 mice and PC12 cells. Our research showed that SA's neuroprotective effect reduced Aβ deposition and cell apoptosis by activating the PI3K/Akt/GSK3β pathway.