l-3-n-Butylphthalide ameliorates β-amyloid-induced neuronal toxicity in cultured neuronal cells

doi:10.1016/j.neulet.2008.01.080

Neuroscience Letters

Volume 434, Issue 2, 28 March 2008, Pages 224-229

https://doi.org/10.1016/j.neulet.2008.01.080 Get rights and content

Abstract

l-3-n-Butylphthalide (l-NBP), as an anti-cerebral ischemia agent, has been shown to have therapeutic effects on learning and memory deficits induced by chronic cerebral hypoperfusion and Aβ intracerebroventricular infusion in rats. In the present study, we investigated the neuroprotective effects of l-NBP on beta-amyloid (Aβ)_25–35-induced neuronal death/apoptosis and potential mechanisms in rat hippocampal neurons and human neuroblastoma SH-SY5Y cells. Aβ_25–35 significantly reduced cell viability and increased the number of apoptotic-like cells, indicating that Aβ_25–35-induced neurotoxicity. In addition, tau protein hyperphosphorylation was found to increase after Aβ exposure. All of these phenotypes induced by Aβ_25–35 were markedly reversed by l-NBP. Pretreatment with l-NBP prior to Aβ_25–35 exposure significantly elevated cell viability, and reduced Aβ_25–35-induced nuclear fragmentation and early apoptosis. Furthermore, immunoreactivity for hyperphosphorylation tau protein was significantly decreased by l-NBP treatment. Our results suggest that l-NBP may protect neurons against Aβ-induced neurotoxicity via inhibiting tau protein hyperphosphorylation.

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l-3-n-Butylphthalide ameliorates β-amyloid-induced neuronal toxicity in cultured neuronal cells

Abstract

FEBS Lett.

Neuron

Neuroscience

Neurosci. Lett.

Neuroscience

Prog. Neurobiol.

Trends Neurosci.

Am. J. Pathol.

DNA damage and apoptosis in Alzheimer's disease: colocalization with c-Jun immunoreactivity, relationship to brain area, and effect of postmortem delay

J. Neurosci.

Effects of chiral 3-n-butylphthalide on apoptosis induced by transient focal cerebral ischemia in rats