Affiliations: Department of Biochemistry, College of Science, King Saud University, Riyadh, Saudi Arabia
Correspondence:
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Corresponding author: Samina Haq, Department of Biochemistry, College of Science, King Saud University, Riyadh, Saudi Arabia. E-mail: shaq@ksu.edu.sa.
Abstract: BACKGROUND:In addition to calcium and phosphate homeostasis in peripheral tissues; vitamin D performs a neuroprotection role in the nervous system. The neuroprotective actions of vitamin D include: increasing vitamin D receptor (VDR) expression, control glutathione synthesis and nitric oxide synthase activity and induce neurotrophins such as nerve growth factor (NGF). VDR mediates cellular actions, and biological responses of the vitamin D. OBJECTIVE:To study the effect of VDR and NGF expression levels by vitamin D3 treatment in induced oxidative stress in primary cortical neuronal cultures. METHOD:Primary neuronal cultures were set up from the cortex region of neonatal rat’s brain. They were cultured for up to 72 h in the presence of 0.25μg/ml vitamin D3. These cells were exposed to 0.5 mM H2O2 for two hours before collecting cell pellet and medium for biochemical assays. Control and H2O2 treated cells were cultured in the absence of vitamin D3 treatment. Sandwich ELISA was used to study NGF expression. Western blotting and immunofluorescence of cultured cells were used to estimate the expression of VDR. RESULTS:Vitamin D3 treatment increased more significantly (P < 0.001) NGF levels with and without induced oxidative stress. Protein expression studies confirmed the positive correlation between VDR expression and vitamin D3 treatment after 72 h in culture. Moreover, pre-treating the cells with vitamin D3 before H2O2 exposure significantly increase (P < 0.05) VDR expression in comparison with the cells exposed to H2O2 alone. CONCLUSION:The neuroprotective effect of vitamin D3 against oxidative stress could be through up-regulating VDR and NGF levels.
