中文摘要：

目的探讨在Aβ25-35诱导的皮层神经元tau蛋白过度磷酸化中,人参皂苷Rb1对周期依赖性蛋白激酶（cyclin-dependent kinase 5,CDK 5）的激动亚基p35/p25的影响.方法通过蛋白免疫印迹法和免疫细胞化学染色法检测胎鼠皮层神经元CDK 5的两个亚基cdk5和p35/p25的蛋白水平,以及CDK 5的磷酸化底物tau蛋白在Ser199/202、Thr205、Ser396和Ser404位点的磷酸化水平.结果凝聚态Aβ25-35 （20 μmol·L-1） 作用于皮层神经元12 h,可使皮层神经元中p25的数量增多,以及tau蛋白在Ser199/202、Thr205、 Ser396和Ser404位点的磷酸化水平增高,但对cdk 5亚基表达水平影响并不明显.Rb1和calpain特异性抑制剂calpeptin可减少皮层神经元p25的生成,同时人参皂苷Rb 1和CDK 5特异性抑制剂roscovitine可减轻凝聚态Aβ25-35诱导的皮层神经元tau蛋白的过度磷酸化水平.结论 p25/cdk 5可能参与人参皂苷Rb1减轻Aβ25-35诱导的tau蛋白过度磷酸化.

英文摘要：

Aim To explore the effect of ginsenoside Rb1 on cyclin-dependent kinase 5 activator, p35/p25 in the process of β-Amyloid peptide 25 -35 -induced tan hyperphosporylation. Methods Western blot and/ or immunocytochemical staining were used to detect the levels of the cyclin-dependent kinase 5 activator-p35/ p25, cdk5 and tan phosphorylation at the sites of Ser199/202 ,Thr205, Ser396 and Ser404 in cortical neurons. Results After exposure to Aβ25-35 （20 μmol . L^-1）for 12 h, the lever of p25 and p25/p35 was increased, but the lever of protein cdk5 did not markly changed. Meanwhile, the levels of tan protein phosphorylation at the sites of Ser199/202, Thr205, Ser396 and Ser404 were also enhanced. Pretreatment with ginsenoside Rbl or calpeptin, a specific inhibitor of calpain, decreased the level of p25. Pretreatment with ginsenoside Rbl or Roscovitine, a specific inhibitor of CDK5, reduced Aβ25-35-induced tau hyperphosphorylation. Conclusion p25/cdk5 may be involved in Ginsenoside Rbl attenuating β-Amyloid peptide 25- 35-induced tau hyperphosporylation.