Document Type : Original Article
Department of Molecular Cell Biology and Genetics, Bushehr Branch, Islamic Azad University, Bushehr, Iran
Department of Genetics, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran
Department of Cell Biology and Genetics, Bushehr Branch, Islamic Azad University, Bushehr, Iran
Farhikhtegan Medical Convergence Sciences Research Center, Farhikhtegan Hospital Tehran Medical Sciences, Islamic Azad University, Tehran, Iran
Objective: Parkinson’s disease (PD) is a severely debilitating disease for which no suitable treatment has been found
so far. In recent years, nanoparticles (NPs) have shown therapeutic potential in PD. Thus, in the current research, for
the first time, we investigated the effects of vitamin E and TiO2 nanoparticles (TiO2-NPs) on a rat model of PD.
Materials and Methods: In this experimental study, after preparation and induction of PD, rats were administrated
with vitamin E and TiO2-NPs. One day after receiving the last dose of treatments, rats were killed and substantia
nigra was extracted from the brain and its cell suspension was prepared. In each group, female rats were mated, and
after confirmation that the female rats were pregnant by vaginal smear test, the fetus was removed. Cell viability was
studied by the MTT method and apoptosis, and necrosis were studied by the flow cytometry technique. Also, after RNA
extraction and cDNA synthesis, the expression of Bcl-2 and circRNA 0001518 genes were studied using the real time
polymerase chain reaction (RT-PCR) technique. For analyzing the data, two-way ANOVA was used.
Results: The results showed a sharp decrease in cell viability in female PD rats and fetuses resulting from PD female
rats. Vitamin E treatment showed the greatest effect on increasing cell viability. Decreased expression of the Bcl-2 gene
and increased expression of circRNA 0001518 were observed in PD conditions.
Conclusion: Administration of vitamin E may be a good option for reducing PD-induced cell death.