Cerebral Ischemia and Estrogen Role: A Review about Classification, Experimental Models, Mechanism of Neural Cell Death after Ischemia and Estrogen Role in Ischemia

Shimaa Mohamed,Amany Ahmed,Shahira Nofal,Engy Elmorsy

doi:10.21608/aprh.2019.7791.1077

Abstract

Cerebral ischemia is a neurovascular disease in which blood flow to the brain decreases which leads to glucose and oxygen deprivation in the brain and this finally results in neuronal cell death. On the other hand, it was found that reperfusion augments this damage by increasing availability of oxygen. Cerebral ischemia can be classified into two major categories as focal and global cerebral ischemia. The mechanisms of neural cell damage following cerebral ischemia reperfusion is complex cascade, which ultimately leads to cell apoptosis or necrosis following disturbance in ion distribution, excitotoxicity, oxidative stress, and, mitochondrial dysfunction. The incidence of stroke is higher in postmenopausal women than premenopausal ones and it was found that they suffer from more severe side effects than men in matched age. It was found that estrogen has neuroprotective actions against cerebral ischemia in both male and ovariectomized rats via various mechanisms as antioxidant, anti-inflammatory, nootropic, and glucose transporters enhancing beside activation of survival signal transduction pathway either genomic or non-genomic.

Highlights

Cerebral ischemia is one of the most leading reasons of mortality worldwide; clinical investigations continue to identify the likely effects of various compounds on cerebral ischemia
Cerebral ischemia, which happens as a result of inadequate blood flow, leads to permanent death of the neuronal cell1.Stroke is known as the second cause of death and the third cause of disability 2
In ischemic stroke, which is about 80% of all strokes, reduced or abolished circulating blood, deprives neurons of main substrate 4, which is divided into embolic in which blood flow is blocked by presence blood clots in arteries; clots travel from heart through the blood stream to brain, or thrombolic in which blood flow is impaired because of fat deposits which cause http://aprh.journals.ekb.eg/ 90

Summary

INTRODUCTION

Cerebral ischemia is one of the most leading reasons of mortality worldwide; clinical investigations continue to identify the likely effects of various compounds on cerebral ischemia. The target artery can be occluded by many ways namely; mechanical compression, cauterization, injection of a photosensitizing dye (e.g. Rose Bengal) with simultaneous laser irradiation, injection of carbon microsphere, intraluminal occlusion by insertion of a nylon thread or injection of platelet aggregate or small blood clots This model is the most widely used in rat stroke owing to its simplicity and non-invasiveness. When ET-1 is injected to the MCA there is obvious reduction in the cerebral blood flow (CBF) in its area, causing an ischemic lesion similar to the direct MCAO 65 This model may be beneficial in restorative drug researches. Surgical focal cerebral models are invasive, and they need craniotomy which exposes the brain to the atmosphere and affects intracranial pressure and blood brain barrier(BBB) function in addition damage to the surrounding autonomic nerves caused by clipping or cauterization of the MCA 66. 3- Excitotoxicity In vitro models permit study of excitotoxicity in isolation of ischemic damage, through application of glutamate receptor agonists such as N-Methyl-Daspartate (NMDA) or glutamate

Mechanisms of brain injury following cerebral ischemia and reperfusion

Anti-Inflammatory Effects of estrogen

Findings

CONCLUSION