Protective Role of Curcumin on Apoptosis Levels in Sodium Azide-Induced Stress Model in SH-SY5Y Cells

Abstract

Oxidative stress, impairments of cellular ATP production and changes in membrane integrity of mitochondria are components of mitochondrial dysfunction and are cross borders of several neurodegenerative diseases. Sodium azide is a chemical agent targeting mitochondrial oxidative phosphorylation and widely used in experimental stress models and hypoxia in neuronal cells. Therefore, in this study it was aimed to investigate the possible role of curcumin on changes in molecular pathways in SH-SY5Y cells induced by SA by using different biochemical methods. SA-gene interactions analyses were done with The Comparative Toxicogenomics Database. Pathway analysis was studied with Enrichr. Dose determination of SA was done with MTT cell viability assay and after that apoptosis, mitochondrial membrane depolarization and intracellular reactive oxygen species production assays were performed in study groups. In this study, it has been shown that the SA model of mitochondrial stress can be decreased by curcumin treatment. Curcumin administration reverses cell death and decrease mitochondrial depolarization levels. However, it seems that curcumin may also be insufficient to decrease intracellular reactive oxygen species production. Thus, combined therapeutic approaches enhancing mitochondrial antioxidative capacity are thought to elucidate potential role of curcumin on SA-induced stress model in SH-SY5Y neuronal cells.