Abstract
The accumulation of β amyloid (Aβ) and intracellular tau protein hyperphosphorylation in the brain are the major pathological features of Alzheimer's disease (AD), leading to neuron dysfunctions and brain cell apoptosis. Vit.D has been shown to promote cell survival through increasing the expression of GDNF. In this study, we investigated the preventive effects of 1,25(OH)2D3 on Aβ‐induced toxicity to SH‐SY5Y human neuroblastoma cells. 1,25(OH)2D3 was pre‐treated to the cells at concentrations of 0.1, 1, 10, and 100 nM 24 hours before 24 hours Aβ (1 μM) treatment. It was found that 1,25(OH)2D3 increased GDNF protein expression, activated the phosphatidylinositol 3 kinase/protein kinase B (PI3K/Akt) pathway and decreased cell tau protein hyperphosphorylation and apoptosis in SH‐SY5Y cells treated with Aβ after the 1,25(OH)2D3 pre‐treatment. In conclusion, 1,25(OH)2D3 showed potentials in protecting the detrimental effects caused by Aβ in neuronal cells.
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