Perindopril Possesses a Protective Impact on Neuronal Function by Lowering Inflammation and Oxidative Stress in Adult Male Rats During Ischemia/Reperfusion

Abstract

Background: Cerebral ischemia/reperfusion (CI/R) is a separate feature of ischemic stroke that occurs when blood perfusion is restored following a period of ischemia. Despite the beneficial effects of reperfusion, it can cause even more harmful outcomes than persistent ischemia. Objectives: This study was conducted to assess perindopril's neuroprotective ability in (CI/R) and to conceptualize its molecular underpinnings. Materials and Methods: The 28 Sprague-Dawley male rats weighing 200-300 g were randomly divided into four groups, each with seven rats: Sham (undergo general anesthesia without bilateral common carotid artery occlusion (BCCO)), Control (30 min. of BCCO followed by reperfusion 60 minutes), Vehicle (7 days of distilled water then as control group), and Perindopril-treated group (7 days of Perindopril-treated then as control group). After reperfusion, the brain's tissues were extracted in order to evaluate the levels of biochemical, and total antioxidant capacity in addition to the extent of the infarct and histological investigation. Results: Cerebral infarct size, as well as levels of inflammatory marker were significantly higher in the control and vehicle groups compared to the sham groups, although overall anti-oxidant capability was significantly lower. Perindopril therapy increased IL-10 and overall antioxidant capacity while decreasing IL-6, TNF-\(\alpha\), NF-kB p65, and ICAM-1 significantly. Histopathological, both control and vehicle rats had severe ischemia damage, which was significantly alleviated by perindopril therapy. Conclusions: The perindopril neuroprotective effect in rats exposed to cerebral ischemia/reperfusion injury may be attributed to the anti-inflammatory and anti-oxidative effect of perindopril.