Effect of Ischemic Postconditioining on Change of Immunoreactivity Level to PECAM-1/CD31 in Rat Neocortex Structures after Global Brain Ischemia

Abstract

Introduction. Ischemic postconditioning (IPostC) of the brain can be considered as a promising approach to limit reperfusion injury in the ischemic area of the brain. Objective – to study the effect of IPostC after global cerebral ischemia on the level of immunoreactivity to PECAM-1/CD31 in the structures of layers II, III and V of the neocortex of rats at different periods of the reperfusion period.Material and methods. In male Wistar rats, a 10-minute global cerebral ischemia was modeled followed by IPostC in the form of reperfusion-ischemia at 15sec/15sec. In the early (2 days) and late (7 days) reperfusion periods after damaging ischemia, the number of morphologically unchanged neurons and the level of immunoreactivity to PECAM-1/CD31 in the structures of layers II, III and V of the neocortex were estimated.Results. It is shown that the use of IPostC by 2 days of reperfusion contributed to the increase in the number of unchanged neurons in layers II and III of 25.8 and 28.2 % (P<0.05), which was not accompanied by changes in the level of immunoreactivity to PECAM-1/CD31, to 7 days of reperfusion there was an increase in the number of unchanged neurons in layers II, III and V of 19.2, 22,1, 21,4 % (P<0.05) was observed a decrease in the level of immunoreactivity to PECAM-1/CD31 in the structures of these layers of 27.4, 39.4, and 16.7 % (P<0.05), respectively, when compared with similar indicators in groups without the use of IPostC.Conlusions. In the mechanisms of physiological reaction formed in the application of ischemic postconditioning after cerebral ischemia and leading to the preservation of the number of unchanged neurons in the late reperfusion period involved PECAM-1/CD31, which suggests that the protective potential of the phenomenon is realized by possible inhibiting the migration of neutrophils, monocytes and lymphocytes and extravasation of leukocytes from the systemic blood flow into the damaged area of the brain, i.e. through suppression of inflammatory response.