Effect of ischemic postconditioining on reaction of neocortex microglia after global brain ischemia in rats

Abstract

Introduction. Ischemic postconditioning (IPostC) is a new concept in the brain protection strategy. Almost all researches in this area focus on the functioning and survival of neurons, while non-neuronal cells affected by IPostC remain unexplored.The aimis to study the IPostC effect on changes in microglia in the neocortex of Wistar rats after global brain ischemia during various periods of reperfusion.Materials and methods. Male Wistar rats were used as a model of a 10-minute global brain ischemia with a subsequent IPostC; the reperfusion-ischemia cycle was 15 s/15 s. In the early (2 days) and late (7 days) reperfusion periods, the number of morphologically unchanged neurons and Iba-1-positive nucleated microglyocytes in the occipital cortex was estimated.Results. It has been shown that global brain ischemia in rats leads to 25.9% (P<0.05) neuron death and an increase of 30.9% (P<0.05) in the number of Iba-1-positive microglia cells by the 2nd day of the reperfusion period in the occipital neocortex; by the 7th day of reperfusion, there was observed a neuron death significant increasing by 34.5% (P<0.05) and the number of Iba-1-positive microglia cells increasing of 65.2% (P<0.05) compared to similar indicators in sham-operated groups. The IPostC by 2 days of reperfusion was found to increase the number of unchanged neurons in the occipital region of the cerebral cortex by 18.3% (P<0.05), which is not accompanied by a significant change in the number of Iba-1-positive microglial cells; by 7 days of reperfusion the increase number of unchanged neurons was found to be 23.5% (P<0.05) in the analysed brain region , which is accompanied by a decrease in the number of Iba-1-positive microgliosis by 32.5% (P<0.05) comparing with similar indicators in groups without IPostC.Conlusions. The results of this work suggest that the cytoprotective effect of IPostC for neurons of the occipital neocortex of Wistar rats in the long-term reperfusion period is caused by blocking the infiltration of the ischemic brain region by both resident and recruited cells of the immune system.