人参皂苷Rb1减轻β-淀粉样肽25-35诱导的皮质神经元tau蛋白过度磷酸化

[Ginsenoside Rbl attenuates beta-amyloid peptide25-35 -induced tau hyperphosphorylation in cortical neurons].

作者信息

Zeng Yu-qi, Chen Xiao-chun, Zhu Yuan-gui, Li Yong-kun, Peng Xiao-song, Chen Li-min, Shen Jie, Huang Tian-wen

机构信息

Fujian Institute of Geriatrics, the Affiliated Union Hospital of Fujian Medical University, Fuzhou 350001, China.

出版信息

Yao Xue Xue Bao. 2005 Mar;40(3):225-30.

PMID:15952593

Abstract

AIM

To explore the effect and the possible mechanism of ginsenoside Rb1 on beta-amyloid peptide (beta-AP)(25-35) -induced tau protein hyperphosphorylation in cortical neurons.

METHODS

Western blotting and immunocytochemical staining were used to detect tau phosphorylation level, total tau and glycogen synthase kinase-3beta (GSK-3beta) in cortical neurons.

RESULTS

After exposure to beta-AP(25-35) (20 micromol x L(-1)) for 12 h, the levels of tau protein phosphorylation in the sites of Ser 396, Ser 199/202, Thr 231 and total tau were raised. Meanwhile, the expression of GSK-3beta also increased. Pretreatment with ginsenoside Rbl or lithium chloride, a specific inhibitor of GSK-3beta, markedly reduced beta-AP(25-35)-induced tau hyperphosphorylation and the expression of GSK-3beta.

CONCLUSION

Ginsenoside Rb1 can attenuate beta AP(25-35)-induced tau protein hyperphosphorylation in cortical neurons by inhibiting the expression of GSK-3beta.

摘要

目的

探讨人参皂苷Rb1对β-淀粉样肽（β-AP）（25-35）诱导的皮质神经元tau蛋白过度磷酸化的影响及其可能机制。

方法

采用蛋白质免疫印迹法和免疫细胞化学染色法检测皮质神经元中tau蛋白磷酸化水平、总tau蛋白及糖原合成酶激酶-3β（GSK-3β）。

结果

用β-AP（25-35）（20 μmol·L⁻¹）处理12 h后，Ser 396、Ser 199/202、Thr 231位点的tau蛋白磷酸化水平及总tau蛋白水平升高。同时，GSK-3β的表达也增加。用人参皂苷Rb1或GSK-3β的特异性抑制剂氯化锂预处理，可显著降低β-AP（25-35）诱导的tau蛋白过度磷酸化及GSK-3β的表达。