Objective: To investigate the neuroprotective effect of modified Wuzi Yanzong prescription (MWP)on β-amyloid protein (Aβ25-35)-induced tau protein hyperphosphorylation in PC12 cells and the potential mechanism. Method: Control

Aβ25-35 model and sample treatment groups were set in our study. Aβ25-35(30 μmol ·L-1)was used to induce tau protein hyperphosphorylation in PC12 cells

and MWP(50-400 mg ·L-1)was also simultaneously added. Then

the neuroprotective effects of MWP were investigated. Result: MWP alone did not show any cytotoxicity in PC12 cells. MWP significantly protected PC12 cells from Aβ25-35-induced neurotoxicity

cell viability increased from (70±4.9)% to (98±6.5)%(P<0.01)

and apoptosis-related protein (Caspase-3 and PARP)expressions were also effectively inhibited

Caspase-3 and PARP were down-regulated from (378.15±34.65)% and (985.12±45.32)% to (127.65±12.65)% and (543.61±39.07)%(P<0.01). In addition

tau protein hyperphosphorylation in PC12 cells was significantly down-regulated

p-tau (in Ser396 site) expression decreased from (130.01±5.83)% to (113.75±6.34)%(P<0.01)

and p-tau (in Ser404 site) expression decreased from (150.17±10.28)% to (105.37±4.57)%(P<0.01). The inhibitory effects of MWP on the phosphorylation of glycogen synthase kinase 3β(GSK-3β)at Ser9 site and mitogen-activated protein kinases (MAPK) may explain the potential mechanism. Conclusion: MWP could inhibit Aβ25-35-induced tau protein hyperphosphorylation on PC12 cells

showing a neuroprotective effect in Alzheimer’s disease.