Paradoxical mitochondrial effects of nitric oxide synthase inhibition following oxygen-glucose deprivation-reoxygenation (OGD/R) in endothelial cells and neurons.
Investigation of nitric oxide synthase inhibition shows differing effects on mitochondria in endothelial cells and neurons, suggesting new therapeutic targets.
Key Points
NOS inhibition enhances survival in both BMECs and neurons after injury, indicating a protective role.
Post-OGD/R, mitochondrial respiration decreases in both cell types due to NOS inhibition, showing a paradoxical response.
Cell viability was assessed via Cell Counting Kit-8, indicating the effectiveness of the NOS inhibition.
Mitochondrial effects diverged under normoxia, with reduced respiration in BMECs but increased oxygen consumption in neurons.