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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Rg1对tau蛋白过度磷酸化及周期依赖性蛋白激酶5(CDK5)的激动亚基p35的影响。方法通过蛋白免疫印迹法检测胎鼠皮层神经元CDK5的两个亚基cdk5和p35/p25的蛋白水平,以及CDK5的磷酸化底物tau蛋白在Thr205和Ser404位点的磷酸化水平。结果凝聚态Aβ25-35(20μmol/L)作用于皮层神经元12h,皮层神经元中p35裂解成p25的数量增多,tau蛋白在Thr205和Ser404位点的磷酸化水平增高,对cdk5亚基表达水平的影响不明显。人参皂苷Rg1和calpain特异性抑制剂calpeptin可稳定皮层神经元的p35蛋白,减少p25生成,人参皂苷Rg1和CDK5特异性抑制剂roscovitine可减轻凝聚态Aβ25-35诱导的皮层神经元tau蛋白过度磷酸化。结论CDK5可能参与人参皂苷Rg1减轻寡聚态Aβ25-35诱导的皮层神经元tau蛋白过度磷酸化。
Objective To investigate the effect of ginsenoside Rg1 on the hyperphosphorylation of tau and the activation subunit p35 of CDK5 in the hyperphosphorylation of tau protein in cortical neurons induced by Aβ25-35. Methods The protein levels of CDK5 subunits cdk5 and p35/p25 in fetal rat cortical neurons and the phosphorylation level of phosphorylated substrate tau of CDK5 at Thr205 and Ser404 were detected by Western blotting. RESULTS: Condensed Aβ25-35 (20 μmol/L) acted on cortical neurons for 12 h. The number of p35 cleavage into p25 in cortical neurons increased, and the phosphorylation of tau at Thr205 and Ser404 increased, and the expression level of cdk5 subunits increased. The effect is not obvious. Ginsenoside Rg1 and calpain specific inhibitor calpeptin can stabilize the p35 protein of cortical neurons and reduce the production of p25. Ginsenoside Rg1 and CDK5 specific inhibitor roscovitine can reduce the aggregation of Aβ25-35-induced hyperphosphorylation of tau protein in cortical neurons. . Conclusion CDK5 may be involved in ginsenoside Rg1 to reduce tau hyperphosphorylation in oligo-state Aβ25-35-induced cortical neurons.