STUDY THE EFFECT OF ROSUVASTATIN , AMLODIPINE AND THEIR COMBINATION IN EXPERIMENTAL INDUCED ACUTE CEREBRAL ISCHEMIA IN MALE RATS.
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Cerebral ischemia is a major leading cause of death and at the first place cause of disability all over the world There are a lot of drugs that are in experimental stage for treatment of stroke. A mong them are statins and calcium channel blockers that have, in animal models, dfferent effectiveness in healing of ischemic damage in brain. Their mechanisms in cerebral ischemia is still unclear, but antioxidative, antiinflammatory and neuroprotective properties is supposed to be implicated In the present study, we investigated antioxidant, anti-inflammatory and neuroprotective properties of HMG-CoA reductase inhibitor (Rosuvastatin) and calcium channel blocker (Amlodipine). Methods administration of Rosuvastatin (20mg/kg/Ip) and Amlodipine (3.2mg/kg/lp) just after induction of cerebral ischemia in male albino rats. Cerebral ischemia was induced by temporary occlusion of left common carotid artery for 60 min. ,then stroke index(SI) was calculated at day 4 after ischemia, behavioral test (cyclic & placing test) were performed Rat were sacrified and area of cerebral infarction was measured serum superoxide dimutase (SOD) enzyme, glutathione peroxidase (GHPx), Malondihydryde (MDA), C-reactive protein(CRP)and total cholesterol level were also measured The present result reveald that vehicle ischemic group produced high stroke index, extensive cerebral infarction and behavioral deficit. Also, it significantly decreased serum SOD, GHPx, and increased MDA, CRP. treatment with Rosuvastatin and Amlodipine significantly ameliorated SI, cerebral infarction, behavioral deficit, SOD, GHPx, MAD, CD without affection of serum cholesterol level. This improvement was more pronounced in the group receiving both drugs together. These findings suggest that Rosuvastatin and Amlodipine have neuroprotective effect against cerebral ischemia induced behavioral deficit and neuronal degeneration that may be mediated through antioxidant, anti-inflammatory mechanisms in normocholesterolemic rats.