Effects of EGCG on nerve protection and BACE1 expression level in hippocampus of mice with Alzheimer's disease

Objective To explore neuroprotective effects of epigallocatechin-3-gallate(EGCG)and its influence on levels of beta-site amyloid precursor protein-cleaving enzyme 1(BACE1) and Tau protein phosphorylation in hippocampus of mice with Alzheimer's disease.Methods We adopted senescence-accelerated mouse prone-8(SAMP8) as Alzheimer's disease(AD)animal model;we usded Morris water maze to measure learning and memory function of the mice and real-time quantitative reverse transcriptase polymerase chain reaction(qRT-PCR)and Western blot to investigate neuroprotective effect of EGCG and its influence on levels of BACE1 expression and phosphorylation of TAU S202 and S396.Results Compared to those of SAMR1 mice(a strain of resistant to senescence),the escape latency(49 ±2.98 s) prolonged and target quadrant residence time(13.52 ±3.11 s)was shortened in SAMP8 group5 days after the training(P 0.05 for all).Compared with those of the SAMP8 group,the escape latency(41 ± 3.03 s)was shortened and target quadrant residence time(25.47 ± 4.78 s) was prolonged in EGCG-treated group(P 0.05).The results of qRT-PCR and Western blot showed that the BACE1 level(2.835 ± 0.902 for P8 and 1.574 ± 0.556 for EGCG group)was down-regulated and the phosphorylation level of TAU S202 and S396 decreased remarkably after EGCG treatment.Conclusion EGCG reduces BACE1 expression and TAU phosphorylation level and the neuroprotective effect of EGCG provides a new strategy for Alzheimer's disease prevention and treatment.