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Indirubin-3′-monoxime inhibits β-amyloid-induced neurotoxicity in neuroblastoma SH-SY5Y cells

Authors
Journal
Neuroscience Letters
0304-3940
Publisher
Elsevier
Publication Date
Volume
450
Issue
2
Identifiers
DOI: 10.1016/j.neulet.2008.11.030
Keywords
  • Indirubin-3′-Monoxime
  • Alzheimer'S Disease
  • Neuronal Apoptosis
  • Tau Protein Hyperphosphorylation
Disciplines
  • Biology
  • Medicine
  • Pharmacology

Abstract

Abstract Increasing evidence suggests that the inappropriate activation of cyclin-dependent kinases (CDKs) could induce neuronal apoptosis in Alzheimer's disease (AD), which means that the pharmacological inhibitors of cell-cycle progression may effectively impede the development or progression of AD. Indirubin-3′-monoxime (IMX), a known effective inhibitor of CDKs, has been shown to have therapeutic effects on learning and memory deficits induced by beta-amyloid (Aβ) intracerebroventricular infusion in rats. In the present study, we investigated the neuroprotective effects of IMX on Aβ25–35-induced neuronal apoptosis and its potential mechanisms in human neuroblastoma SH-SY5Y cells. Aβ25–35-induced apoptosis, characterized by decreased cell viability, neuronal DNA condensation, and fragmentation, was associated with an increase in tau protein hyperphosphorylation. IMX, however, attenuated Aβ25–35-induced cell death in a dose-dependent manner. Furthermore, expression of hyperphosphorylation tau protein was significantly decreased with IMX treatment. Our study suggests that IMX may usefully prevent or delay the neuronal loss of AD.

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