人参皂苷Rb1可能通过CDK5途径减轻Aβ_(25-35)诱导的胎鼠海马神经元tau蛋白过度磷酸化

Ginsenoside Rb1 attenuates β-amyloid peptide_(25-35)-induced hyperphosphorylation of tau protein through CDK5 signal pathway

观察人参皂苷Rb1对Aβ25-35诱导的海马神经元tau蛋白过度磷酸化的影响,并探讨其对周期依赖性蛋白激酶(cyclin-dependent kinase 5,CDK5)及激动亚基p25/p35的可能作用。通过蛋白免疫印迹法和免疫细胞化学染色法检测胎鼠海马神经元tau蛋白在Thr205、Ser396和Ser404位点的磷酸化水平,及CDK5的两个亚基cdk5和p25/p35的蛋白水平。20μmol.L-1凝聚态Aβ25-35作用于海马神经元12 h,可使海马神经元tau蛋白在Thr205、Ser396和Ser404位点的磷酸化水平增高,p25的数量增多,但并不影响cdk5亚基的表达。人参皂苷Rb1可减轻凝聚态Aβ25-35诱导的海马神经元tau蛋白的过度磷酸化,抑制p35的降解并减少海马神经元p25的生成。人参皂苷Rb1可能通过CDK5途径减轻Aβ25-35诱导的胎鼠海马神经元tau蛋白过度磷酸化。

This study is to explore the effect of ginsenoside Rb1 on the process of β-amyloid peptide_(25-35)(Aβ_(25-35))-induced hyperphosphorylation of tau protein,and on the level of cyclin-dependent kinase 5 activator,p25/p35.Western blotting and/or immunocytochemical staining were used to detect the levels of phosphorylation of tau protein at the sites of Thr^(205),Ser^(396),Ser^(404) in hippocampal neurons, cdk5 and p25/p35.After exposure to Aβ_(25-35)(20 μmol·L^(-1)) for 12 h,the levels of tau protein phosphorylation at the sites of Thr^(205),Ser^(396),Ser^(404) were enhanced,the level of p25 was increased,but the level of protein cdk5 was not changed markedly.Pretreatment with ginsenoside Rb1 reduced Aβ_(25-35)-induced hyperphosphorylation of tau protein and decreased the lever of p25,but had no effect on cdk5.Ginsenoside Rb1 can attenuate Aβ_(25-35)-induced hyperphosphorylation of tau protein through CDK5 signal pathway.