Introduction. One of the main causes of mortality and disability of people in the whole world is disorders of cerebral circulation. Meanwhile, against the ground of disorders of cerebral microcirculation energy deficiency, lactate acidosis, oxidative stress and cellular death occur. Although, genome reaction plays one of the main roles in pathogenesis of cerebral disorders; р53+ gene associated with triggering programmed cellular death is of special interest.
Objective. To study the influence of incomplete global cerebral ischemia in dynamics with further reperfusion of various duration on the peculiarities of apoptosis of the nerve and glia cells of the frontal area of the cerebral cortex in male rats.
Materials and methods. Ischemia-reperfusion was modeled in laboratory rats. After that the cortex of the frontal cerebral area was taken, fixed in 10% Bouin’s solution, coated with paraffin blocks, and histological cuts were prepared 5 mcm thick and incubated with monoclonal antibodies to р53+ gene. The processed histological cuts were examined by means of the computed system of digital analysis of VIDAS-386 image.
Results of the research. Bilateral carotid ischemia-reperfusion was found to cause the increase of location density and percentage of р53+ nerve cells in the cortex of the frontal cerebral area, and the percentage of р53+ glia cells on the 12th day of ischemic-reperfusion period. Ischemic-reperfusion lesion of the brain disturbs morphometric parameters of р53+ nerve and glia cells of the cortex in the frontal cerebral area both in early and late periods of observation.