中文摘要：

目的：研究加味五子衍宗方对β-淀粉样蛋白（β-amyloid protein,Aβ25-35）所致的大鼠肾上腺嗜铬细胞瘤细胞株（PC12）中的微管相关蛋白（tau蛋白）高度磷酸化的抑制作用和潜在机制。方法：将PC12细胞分为正常对照组、模型组、给药组,使用Aβ25-35（30μmol.L-1）诱导PC12细胞的tau蛋白高度磷酸化,并同时加入加味五子衍宗方提取物（50～400 mg.L-1）作用细胞24 h,然后考察加味五子衍宗方对PC12细胞tau蛋白高度磷酸化的抑制作用。结果：加味五子衍宗方单独作用细胞后,无明显毒性作用。但是加味五子衍宗方可以显著的抑制Aβ25-35所诱导的神经毒性,细胞存活率由损伤组的70%±4.9%提高到治疗组的98%±6.5%（P〈0.01）;且凋亡相关蛋白Caspase-3和PARP的表达也受到了显著性的抑制,分别从损伤组的378.15%±34.65%和985.12%±45.32%降低到治疗组的127.65%±12.65%和543.61%±39.07%（P〈0.01）。此外,PC12细胞中tau蛋白的高度磷酸化也出现了显著下调,Ser396位点的磷酸化水平从损伤组的130.01%±5.83%降低到治疗组的113.75%±6.34%（P〈0.01）,Ser404位点的磷酸化水平从损伤组的150.17%±10.28%降低到治疗组的105.37%±4.57%（P〈0.01）,其机制可能是通过抑制糖原合酶激酶（glycogen synthase kinase 3β,GSK-3β）在Ser9位点的磷酸化以及促分裂素原活化蛋白激酶（mitogen-activated protein kinases,MAPK）的磷酸化来实现的。结论：加味五子衍宗方可以有效的抑制Aβ25-35所致的PC12细胞中tau蛋白的高度磷酸化,具有潜在的治疗阿尔茨海默病的作用。

英文摘要：

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,cellviability 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.