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1,25(OH)2D3 Protects SH‐SY5Y Human Neuroblastoma Through Decreasing Aβ Toxicity and Reducing Tau Protein Hyperphosphorylation
Author(s) -
Liao Hsiang,
Chang YiChen,
Lin ShyhHsiang
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.636.25
Subject(s) - sh sy5y , hyperphosphorylation , protein kinase b , apoptosis , tau protein , neuroblastoma , glial cell line derived neurotrophic factor , chemistry , kinase , pi3k/akt/mtor pathway , protein kinase a , microbiology and biotechnology , biology , medicine , alzheimer's disease , neurotrophic factors , cell culture , biochemistry , receptor , disease , genetics
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) 2 D 3 on Aβ‐induced toxicity to SH‐SY5Y human neuroblastoma cells. 1,25(OH) 2 D 3 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) 2 D 3 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) 2 D 3 pre‐treatment. In conclusion, 1,25(OH) 2 D 3 showed potentials in protecting the detrimental effects caused by Aβ in neuronal cells.