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Background:Stroke is a highly troubling disorder with a high mortality rate, it is considered as a second predisposing cause of death and deficit wide word. Restriction of cerebral blood flow can disturb cellular homeostasis due to insufficient oxygen and nutrient delivery. However, the re-establishment of cerebral blood flow can aggravate the impairment of ischemic brain tissue contributing to a series of oxidative, inflammatory events resulting in cerebral ischemia-reperfusion (CI/R) injury, which eventually results in neuronal death and neurological disability.
Method: An experimental model of 30 Sprague-Dawley rats were randomly allocated to five groups, sham group, I/R group, I/R+(DMSO as a vehicle), I/R+ intraperitoneal (i.p) Empagliflozin 5mg/kg 1 hour before induction of BCCAO, and I/R+intraperitonealEmpagliflozin 10mg/kg 1hour before induction of BCCAO.
Results:histopathological examination showed that Empagliflozin ameliorated the histological lesions induced by CI/R. Besides, the assessment of cerebral infarction size in each group showed that Empagliflozin reduced the infarction size in both used doses in the study.The immunohistochemical analysis of cerebral tissue expressed that CI/R causesa reduction in neuronal nuclear protein (NeuN protein) in the control and control-vehicle group as compared to sham group,while pre-treatment with Empagliflozin caused re-appearance of NeuN protein in both doses groups.
Conclusions: The study concluded that Empagliflozin has a neuroprotective effect by reduction of cell necrosis and apoptosis due to inhibition of different mechanisms that cause cerebral tissue damage and neuronal death.