中文摘要：

探讨在Aβ25-35（beta-amyloidpeptide（25—35），Aβ25-35）诱导的拟阿尔茨海默病样胎鼠皮层神经元tau蛋白过度磷酸化中，人参皂苷Rbl对tau蛋白磷酸化及JNK／p38 MAPK的可能作用。应用蛋白免疫印迹和免疫细胞化学染色的方法，观察tau蛋白磷酸化和JNK（c-jun N-terminal kinase）／p38MAPK的表达情况。凝聚态Aβ25-35（20nmol·L^-1）作用于皮层神经元12h，tau蛋白的磷酸化水平明显增高，同时JNK／p38MAPK的总量及其活性形式——磷酸化JNK／p38MAPK的蛋白表达水平也增加，人参皂苷Rb1可以减轻tau蛋白的磷酸化水平及JNK／p38MAPK的蛋白水平。人参皂苷Rb1可通过JNK／p38MAPK途径减轻Aβ25-35诱导的tau蛋白过度磷酸化。

英文摘要：

To explore the effect of ginsenoside Rb1 on JNK/p38 MAPK in the process of fl-amyloid peptide （25 -35） -induced tau protein hyperphosphorylation, Western blotting and immunocytochemical stain were performed to observe the tau protein phosphorylation and the expression of JNK/p38 MAPK. The level of tau protein phosphorylation in the sites of Ser39s , Ser199/202 and Thr205 increased after rat cortical neurons exposed to 20μmol·L^-1 Aβ25-35, meanwhile the level of iNK/p38 MAPK also increased after Aβ25-35 treatment for 12 h. Pretreatment with several doses of ginsenoside Rbl markedly attenuated tau protein hyperphosphorylation and the expression of JNK/p38 MAPK. Ginsenoside Rbl markedly attenuated tau protein hyperphosphorylation through JNK/p38 MAPK pathway.