Curcumin attenuates amyloid-β-induced tau hyperphosphorylation in human neuroblastoma SH-SY5Y cells involving PTEN/Akt/GSK-3β signaling pathway

摘要: Accumulated amyloid-β peptide (Aβ) and hyperphosphorylated tau proteins are two hallmarks of Alzheimer's disease (AD). Increasing evidence suggests that Aβ induces hyperphosphorylation in AD pathology, but the signaling pathway is not completely understood. Inhibiting Aβ-induced cellular beneficent to treatment. In this study, phosphorylation induced by inhibiting effects curcumin on were investigated human neuroblastoma SH-SY5Y cells. The results indicated inhibits at Thr231 Ser396, over-expression HDAC6, decrease glycogen synthase kinase-3β (GSK-3β) Ser9. However, protective effect dephosphorylation GSK-3β directly related oxidative stress. Curcumin depresses down-regulation phosphorylations Akt Thr308 Ser473 3-phosphoinositide-dependent protein kinase 1 Ser241, implying second message PIP3 involves curcumin-protective cell signaling. Furthermore, insulin receptor/phosphatidyl inositol 3-kinase pathway, as a regulatory PIP3, does participate deactivation (dephosphorylation Ser473). Phosphatase tensin homolog (PTEN), negative regulator PIP3. up-regulation PTEN Aβ. These imply involving PTEN/Akt/GSK-3β pathway.