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- W2371434062 abstract "Objective To explore whether ginsenoside Rg1 can attenuate β-amyloid peptide 25-35-induced Tau hyperphosporylation in rat embryo cortical neurons by regulating the activity of GSK-3β and PP2A. Methods Primary cultures of cortical neurons were prepared from the embryonic day 18±2 in Sprague-Dawley rats. The experimental groups were designed as follows:1.Neurons culture (control group); 2. Neurons exposed to 20μmol/L Aβ_ 25-35 for 12 hours (Aβ-model group); 3.Neurons exposed to 20μmol/L Aβ_ 25-35 and 10 mmol/L lithium chloride (LiCl), a specific inhibitor of glycogen synthase kinase-3β(GSK-3β), for 12 hours (LiCl group); 4.Neurons exposed to 20μmol/L Aβ_ 25-35 for 12 hours in the presence of 24-hour pretreatment with ginsenoside Rg1 (Rg1 pretreatment group) . Western blotting and immunocytochemical staining were used to detect the levels of Tau phosphorylation,total Tau and GSK-3β in cortical neurons. Non-radioimmunoassay was introduced to detect the activity of protein phosphatase 2A (PP2A). Results In Aβ-model group, the levels of Tau protein phosphorylation in the sites of Ser 396 ,Ser 199/202 ,Thr 231 and total Tau were enhanced. Meanwhile, the expression of GSK-3β was also increased, but the activity of PP2A was unchanged. In LiCl group and Rg1 pretreatment group , the hyperposphorylations of Tau protein and total Tau and the expression of GSK-3β were markedly reduced compared to those of the Aβ-model group (P0.05). 20μmol/L Rg1 pretreatment showed the best protective effect on attenuating Aβ_ 25-35 -induced Tau protein hyperposphorylation and the activity of GSK-3β,and markedly activated the activity of PP2A (P0.01). Conclusion Ginsenoside Rg1 can attenuate β-amyloid peptide 25-35-induced Tau hyperphosporylation in cortical neurons by inhibiting the activity of GSK-3β and activating the activity of PP2A." @default.
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- W2371434062 date "2007-01-01" @default.
- W2371434062 modified "2023-09-24" @default.
- W2371434062 title "THE ATTENUATION OF β-AMYLOID PEPTIDE 25-35-INDUCED Tau HYPERPHOSPORYLATION IN CORTICAL NEURONS BY THE REGULA-TION OF GINSENOSIDE Rg1 ON THE ACTIVITY OF GSK-3β and PP2A" @default.
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