Hiba A Awooda
Al Neelain University, Sudan
Hiba A. Awooda is an Assistant Professor at the Department of Physiology, Faculty of Medicine and Health Sciences, Al Neelain University since 2006. She successfully completed her MSS and Ph.D. in Physiology from Alexandria University (2011) and Al Neelain University (2013) respectively. She teaches physiology to undergraduate medical, dental, physiotherapy and nurse students. She is also a researcher at Al Neelain research center and her interest is to develop biomarkers that are used in the treatment of acute ischemic stroke.
The role of nitric oxide (NO) inhibition in cerebral ischemia/reperfusion (I/R) remains controversial. Rho-kinases (ROCK) are serine-threonine kinases that play a vital role in cell survival, interaction between NO and ROCK isn't clear. Nuclear factor kappa B (NF-β) is a transcription factor that contributes to infarction in experimental stroke. Th is study investigated the potential neuroprotective eff ect of nonselective nitric oxide synthase inhibitor (L-NAME) in rat’s transient cerebral I/R. 30 adult male Wistar rats (150-250 g) were divided into three groups 10 rats in each: First group was sham-operated (control), I/R group of rats infused with 0.9% normal saline intraperitoneally prior to 30 minutes of left common carotid artery occlusion followed by 24-hour of reperfusion and test group infused with L-NAME (15 mg/kg per weight) intraperitoneally 15 minutes prior to the same I/R period. Neurobehavioral assessments were evaluated; NF-β via western blotting and ROCK using ELISA were estimated in the brain tissue. NO metabolites (nitrite and nitrate) were measured colorimetrically in serum and brain tissue. Th e L-NAME group showed a signifi cant improvement in neurological defi cit compared to both I/R and control groups (P<0.001). In I/R group NF-β, NO and ROCK were signifi cantly increased compared to the control group and L-NAME pretreatment resulted in signifi cant decrease of NF-β, NO and ROCK compared to I/R group (P <0.001). Th us, L-NAME signifi cantly improved neurological defi cit and decrease NF-β, NO and ROCK in the aff ected cerebral hemisphere following cerebral ischemic injury.