Neuroprotective effect of sinapic acid in APP/PS1 mouse model and PC12 Cells of Alzheimer's disease via activation of PI3K/Akt/GSK3? signaling pathways

To explore the neuroprotective effects of Sinapic Acid (SA) in APP/PS1 mouse model and amyloid beta-peptide (A?)-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 A?. Western blotting was performed to p-P13K, P13K, p-Akt, Akt, p-GSK3? and GSK3? 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-GSK3?, and GSK3? 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 A? 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/GSK3? in APP/PS1 mice and PC12 cells. Our research showed that SA's neuroprotective effect reduced A? deposition and cell apoptosis by activating the PI3K/Akt/GSK3? pathway.