Ischemia is accompanied by diffuse damage of structural elements of brain: neurons, glia and intercellular contacts. One of the markers that show glial functional processes in nervous system is the S-100 protein.
The objective of the research was to study the changes in the S-100 protein expression in ganglion layer of rat’s brain sensorimotor cortex in cases of modeling of damaged anterior circulation in left carotid artery of different severity degree.
Materials and methods. The study was conducted on 115 male mature white rats of Vistar line weighted 260-290 g, at which the damage of the brain was modulated. The brain for study was taken on 1, 3, 10, 30 and 90 days after the start of the experiment. The histological, immunehistochemical, densitometrical and statistical methods were used.
The damage in brain hemispheres circulation led to changes of S-100 protein expression, direction and degree of which depended on the level of the ischemia.
Practically absolute lack of S-100 expression was observed in infarct focuses. Also, microfocuses with decreased amount of this marker can form, where we suppose degenerative changes caused by ischemia have achieved necrosis.
In saved areas of sensorimotor brain cortex there was a reactive activation of S-100 positive cells that were able to show the long-term processes, demonstrating the post-ischemic reactive gliose phenomenon.
The perspectives of further research in this direction are connected with deepening of understanding of morpho-functional changes in brain at circulatory disorder and also as one of signs for evaluation of severity degree of ischemic damage.
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