Icaritin and icariin reduce p-Tau levels in a cell model of Alzheimer's disease by downregulating glycogen synthase kinase 3β.

Abstract

This study aimed to explore the neuroprotective effect of icariin/icaritin (ICA/ICT) and the role of ICA/ICT in the treatment of Alzheimer's disease (AD). ICA and ICT were used to treat okadaic acid (OA)-induced Tau hyperphosphorylation in SH-SY5Y cells. We detected the relative changes in Tau, p-Tau, protein phosphatase 2A (PP2A), and glycogen synthase kinase 3β (GSK-3β) by Western blotting and enzyme-linked immunosorbent assay. At 40nmol/L OA, the cell viability of the SH-SY5Y cells was significantly changed. We used different concentrations of ICA and IC to treat AD model cells and found that the effect of 2.5μmol/L ICA and 1 μmol/L ICT was best after 48H of treatment. After SH-SY5Y cell induction, the p-Tau levels were increased (P<0.05); after the ICA/ICT treatment, the p-Tau and GSK-3β levels were decreased (P<0.05), although PP2A expression did not change (P>0.05). We found that ICA and ICT exert an effect on AD model cells by decreasing the levels of GSK-3β and p-Tau. The therapeutic effect of ICT is slightly better than that of ICA. Although these drugs were effective in the cell model, more studies are required to determine whether they are promising for the treatment and prevention of AD.