Abstract
Cognitive issues in stroke arise as a result of reperfusion of a clogged artery, which is reported to exacerbate the injury in the brain leading to oxidative stress. Through the present work, we try to understand the regional variations across brain regions mainly cortex and striatum associated with the progression of ischemia-reperfusion injury (IRI). In a rat model of IRI, the influence of varying ischemia and reperfusion times on the biochemical phases across the brain regions were monitored. IRI resulted in the blood-brain barrier disruption and developed mild areas of risk. The brain's tolerance towards IRI indicated a progressive trend in the injury and apoptosis from ischemia to reperfusion that was supported by the activities of plasma lactate dehydrogenase and tissue caspase-3. Cognitive impairment in these rats was an implication of cellular oxidative stress (higher lipid peroxidation and lower antioxidant enzyme activity) that persisted by 24-h reperfusion. The oxidative stress was prominent in the cortex than the striatum and was supported by the lower ATP level. Upregulated Mn-SOD expression leading to a preserved mitochondria in the striatum could be attributed to the regional protection. Overall, a progression of IRI was observed from striatum to cortex leading to 5-day cognitive decline.
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