engleski

Cerebral ischemia and neuroprotection

Cerebral stroke is one of the leading causes of mortality and long-term disability in humans but treatment options are still very limited. Almost 80% of human strokes are of ischemic origin and most of them are caused by middle cerebral artery occlusion (MCAO). In experimental conditions, this model is widely recognized as a reliable and reproducible rodent model of focal cerebral ischemia and reperfusion. Experimentally and clinically, complex pathophysiological cascades of cellular events in ischemic stroke are determined with massive production of reactive oxygene species, leading to either direct injury via membranous lipid peroxidation and protein and DNA oxidation or indirect damage via inflammation and apoptosis. The concept of neuroprotection as potentially valuable adjunct to thrombolytic therapy is based on inhibition of one or more points of ischaemic cascade and reduction of brain damage. In our experimental conditions, focal cerebral ischemia was induced in male Hannover Wistar rats (250- 350 g) by right MCAO model for 1 hr (according to the procedure of DeLonga et al., 1989). After 23 hrs of reperfusion, ischemic animals were sacrificed and the levels of different markers of oxidative stress and inflammation were determined. Ischemic animals received either vehicle or erythropoietin (Epo) (5000 IU/kg, intraperitoneally) immediately or 3 hrs after MCAO, and were sacrificed 23 hrs or 21 hrs later, respectively. Sham operated, vehicle treated animals served as the control group. Potential effects of Epo treatment on oxidative stress parameters and inflammatory response will be discussed.

Neuroprotection; focal cerebral ischemia; rat

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