The Neuroprotective Effect of Sodium Nitrite on Ischemic Stroke-Induced Mitochondrial Dysfunction via Downregulation of Intrinsic Apoptosis Pathway

Objective: Ischemic stroke leads to programmed cell death via intrinsic mitochondrial apoptosis pathways. Nitric oxide donors (NODs) are various kinds of drugs with the ability to produce nitric oxide (NO) as a potential bioregulator of apoptosis. Therefore, we aimed to evaluate the effect of sodium nitrite (SN) on ischemic injury-induced mitochondrial damage. Materials and Methods: A 4-hour oxygen-glucose deprivation (OGD) cellular model was developed to mimic cerebral ischemia injury. Cell viability was determined to demonstrate the efficiency of SN as a NO donor on OGD injured PC12 cells. Immunoblotting was performed to measure the expression of Bcl2, Bax and cleaved caspase 3 proteins. Mito Tracker Green label was used for staining the active mitochondria. Results: The present study confirmed that nitrite inhibited apoptosis via upregulation of Bcl-2 and downregulation of cleaved caspase-3 in OGD-injured PC12 cells as demonstrated by western blot analyses. In addition, nitrite restored mitochondrial vital activity and cell viability in OGD-injured cells. Conclusion: Resultant data illustrated the protective effects of nitrite and may suggest the in vivo use of nitrite for further confirmations.