Abstract: Objective To investigate the effect of proanthocyanidins(PC) induced by amyloid-beta peptide(Aβ_25-35) in human neuroblastoma cell line SH-SY5Y and its possible mechanism. Methods SH-SY5Y cells were exposed to Aβ_25-35 to establish a cell injury model in vitro. PC and(or) secretory protein Dickkopf-1 (Dkk1), the endogenic inhibitor of Wnt/β-catenin signaling pathway were used for intervention. The cells were divided into control group, Aβ_25-35 group, PC(different concentrations)+Aβ_25-35 groups, Dkk1 group, Dkk1+ PC+Aβ_25-35 group.The cell viability was evaluated by MTT assay. The expressions of β-catenin, GSK-3β, p-GSK-3β were measured by Western blot. The secreted Aβ_1-42 was detected by ELISA. Results Compared with the control group, the cell viability, the expression of β-catenin and p-GSK-3β were reduced in Aβ_25-35 treated group(P＜0.05), while the secreted Aβ_1-42 was increased (P＜0.05). PC improved the cell viability, increased the expression of β-catenin and p-GSK-3β, and reduced the secreted Aβ_1-42 in SH-SY5Y cells induced by Aβ_25-35 (P＜0.05). After using Dkk1,the ability of PC was decreased on the enhancement of β-catenin expression, the improvement of p-GSK-3β expression, and the reduction of the secreted Aβ_1-42 (P＜0.05). Conclusions PC may decrease Aβ_1-42 secretion in SH-SY5Y cells induced by Aβ_25-35 through Wnt/β-catenin signaling pathway.

Key words: proanthocyanidins, Aβ_1-42, Wnt/β-catenin