Study and treatment of brain ischemic-reperfusion injury: a morpho-functional approach

Ischemic stroke, caused by impaired blood flow to the brain, remains one of the medical conditions associated with high mortality and long-term disability. Ischemia followed by recanalization of the occluded vessel and restoration of blood flow (reperfusion) is considered an effective therapeutic approach, but reperfusion itself can cause additional injury due to oxidative stress, inflammation, and excitotoxicity. The aim of this study was to examine the morphofunctional state of astrocytes in the penumbra region under conditions of experimental ischemic stroke and subsequent reperfusion. The study was conducted on male Wistar rats using a model of middle cerebral artery occlusion (MCAO) followed by reperfusion. Brain tissue sections were analyzed using immunohistochemistry to detect glial fibrillary acidic protein (GFAP) as a marker of astrocytic activation. In ischemic stroke without reperfusion, astrocytes in the penumbra showed hypertrophy of cell bodies, thickening of processes, and increased GFAP expression. Reperfusion after ischemia led to further activation of astrocytes, characterized by increased cell density, more pronounced hypertrophy, and enhanced GFAP immunoreactivity. These results indicate that reperfusion amplifies astrocytic responses in the penumbra, which may play a dual role: contributing to neuroprotection by maintaining homeostasis, but also participating in the propagation of injury through the release of pro-inflammatory mediators. Understanding the balance between these effects is essential for developing therapeutic strategies aimed at modulating astrocytic activity in the context of ischemic stroke and reperfusion.