|The Neuroprotective Effect of Sodium Nitrite on Ischemic Stroke-Induced Mitochondrial Dysfunction via Downregulation of Intrinsic Apoptosis Pathway.|
|Mohammad Hasan Khadem Ansari1, Pouran Karimi2, Nader Shakib1, Sohrab Minaei Beyrami1|
|1Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran
2Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, Iran
Viewed : 462 times
Downloaded : times.
Keywords : oxygen-glucose deprivation, PC12, nitrite, Bcl2, Bax, mitochondria
|| Related Articles|
Objective: Ischemic stroke leads to programmed cell death via intrinsic mitochondrial apoptosis pathways. Nitric oxide donors (NOD) are the various kinds of drugs with the ability to produce NO (Nitric Oxide) as a potential bioregulator of apoptosis. So we aimed to evaluate the effect of sodium nitrite on Ischemic injury-induced mitochondrial damage.
Materials and Methods: A 4 h oxygen-glucose deprivation (OGD) cellular model was developed to mimic cerebral ischemia injury. Cell viability was determined to demonstrate the efficiency of sodium nitrite 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 to 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. Also, 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 to further confirmations.
Cite By, Google Scholar