Essentially, researchers targeted apoptosis and oxidative stress, two key biological pathways that play a role in the pathogenesis of stroke. The animal model in this study consisted of hypertensive stroke-prone rats.
Oxidative stress is a driving factor behind numerous diseases, including cardiovascular disease and stroke. Methods for attenuating the effect of oxidation is crucial for reducing both the risk for and long-term complications of disease.
A Bruker X-band EPR spectrometer was used to identify reactive oxygen species using spin probe 1-hydroxy-3-carboxy-2,2,5,5-tetramethylpyrrolidine (CPH). An EPR spectrometer by Bruker using the spin trapping technique offers the ability to detect short-lived free radicals in a sample. Using Krebs buffer and 1mmol/L CPH, cells were incubated in situ for a total of 60 minutes for the final hour of the 24-hour period of reoxygenation.
Combined lentivirus-mediated Ngb overexpression was shown to reduce oxidative stress as well as apoptosis significantly in vitro compared to monotherapy after reoxygenation/hypoxia in B50 cells. Infarct volume was also reduced by both JNK inhibition and CAVNgb. The researchers used a 32-point neurologic score to measure the neurologic outcome of the rats after ischemia and found that a combined treatment of CAV, Ngbþ, and JNK inhibition significantly improved neurological function. Also, JNK inhibition and Ngb overexpression reduced the oxidative stress in cultured neurons often associated with reoxygenation/hypoxia.