Abstract
Background:
Alzheimer disease is a progressive neurodegenerative disease, affecting a very high proportion of the aging population. Several studies have demonstrated that one of the main contributors to this disease is oxidative stress (OS), which causes peroxidation of protein, lipids, and DNA resulting in the formation of advanced glycosylated end products (AGE) in the brain tissues. These AGE are usually associated with the amyloid beta (A beta), which could further aggravate its toxicity and its clearance. Antioxidants counteract the deterioration caused by OS.
Objective:
We aimed to evaluate the effect of vitamin D3 and curcumin on primary cortical neuronal cultures exposed to A beta(1-42) toxicity for different time periods.
Methods:
Primary cortical neuronal cultures were set up and exposed to A beta(1-42) for up to 72 hours. Cell viability was studied by 3[4,5-dimethylthiazole-2-yl]-2,5-dipheyltetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assay. Biochemical assays for OS such as lipid peroxidation, reduced Glutathione(GSH), Glutathione S-transferase (GST), catalase, and superoxide dismutase (SOD) were conducted. Sandwich enzyme-linked immunosorbent assay (ELISA) was used to study the neurotrophic growth factor (NGF) expression.
Results:
Treatments with A beta(1-42) caused an elevation in lipid peroxidation products, which were ameliorated in the presence of vitamin D3 and curcumin. Both enzymatic (GST, catalase, and SOD) and nonenzymatic antioxidants (reduced GSH) were raised significantly in the presence of vitamin D3 and curcumin, which resulted in the better recovery of neuronal cells from A beta(1-42) treatment. Treatment with vitamin D3 and curcumin also resulted in the upregulation of NGF levels.
Conclusions:
This study suggests that vitamin D3 and curcumin can be a promising natural therapy for the treatment of Alzheimer disease.