Thesis (M.Sc.) - Cairo University - Faculty of Pharmacy - Department of Pharmacology and Toxicology

Background. Global cerebral Ischemia is one of the leading causes of mortality worldwide. The sudden cessation of blood flow to the brain initiates a cascade of events that leads to severe neuronal brain damage. Allowing reperfusion after ischemia causes further cerebral damage. The neuroprotective effect of cilostazol, a phosphodiesterase inhibitor III, and chrysin, a flavonoid, has not been investigated on global cerebral ischemia, thus it seemed interesting to investigate both drugs in ischemia-reperfusion (I/R) in rats. Methods. Male Wistar rats weighing 200-250 were allocated into four groups. I. Sham-operated control group, II. I/R group subjected to global cerebral ischemia for 15 minutes followed by reperfusion for 60 minutes. Groups III and IV were treated with cilostazol (30 mg/kg p.o.) and chrysin (30 mg/kg p.o.), respectively, for 2 weeks followed by global I/R on the 15th day. Throughout the I/R procedure, rats were subjected to anesthesia with thiopental 30 mg/kg, then they were sacrificed by decapitation. Both hippocampi were rapidly excised to determine the oxidative stress biomarkers: Thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), NADPH oxidase activity and xanthine oxidase (XO) activity and the inflammatory mediators: interleukin 10 (IL-10), interleukin (IL-6) and tumor necrosis factor alpha (TNF-Ü). Apoptotic factors: heat shock protein 90 (HSP 90), Ý-cell lymphoma 2 (BCL-2) and BCL-2 associated X protein (BAX), as well as the excitatory neurotransmitters: glutamate and aspartate, were also evaluated

Issued also as CD