Effect of vitamin D treatment on VDR expression in primary cerebral cortical cells in induced oxidative stress

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.

Expression of vitamin D receptor, CYP24A1, and CYP27B1 in normal and inflamed canine pancreases

“…Moreover, vitamin D could be used to prevent adverse effects caused by VDR reduction in canine pancreatitis. However, research on VDR expression at the protein level, in response to vitamin D administration, is limited to specific cells in certain disorders, such as fibroblasts in human patients with Crohn’s disease ( 36 ) and cerebral cortical cells in oxidative stress ( 37 ). To explore the potential of VDR as a target to treat pancreatitis in dogs, further studies assessing VDR expression and inflammation in the pancreas following vitamin D supplementation would be beneficial.…”

“…However, an increase in CYP24A1 expression in pancreatic tissue is associated with the development of pancreatic ductal adenocarcinoma in humans. This type of adenocarcinoma is explained by reduced 1,25(OH) 2 D activity that regulates tumoral processes such as proliferation, apoptosis, and angiogenesis ( 19 , 37 ). Future research on CYP24A1 expression in canine pancreatic tumor might be beneficial to understand the role of vitamin D metabolism in the pathogenesis of canine pancreatic tumors, a pancreatic disorder that is uncommon but crucial in dogs.…”

“…The present study demonstrated that VDR expression is decreased in canine pancreatitis and suggests that VDR could be a potential target to treat pancreatitis in dogs. Previous studies revealed that supplementation of vitamin D increases VDR mRNA expression and VDR protein levels (35)(36)(37). Moreover, vitamin D could be used to prevent adverse effects caused by VDR reduction in canine pancreatitis.…”