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

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.
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.
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.
Resultant data illustrated the protective effects of nitrite and may suggest the in vivo use of nitrite for further confirmations.