Експресія tau-протеїну в сенсомоторній корі великих півкуль при моделюванні транзиторної ішемії на фоні попе-редньої сенсибілізації мозковим антигеном та імунокорекція виниклих змін

Abstract

Introduction. Ischemic brain damage may was caused by a violation of synaptic transmission after primary thromboembolism. One of the proteins, synaptic pulse transfer and axonal transport is tauprotein. The scientific literature has extensively studied the detection of tau protein in Alzheimer's disease, and is practically was not described in cases of ischemic brain damage in conditions influencing the body of immunomodulator of the new generation. Therefore, the purpose of the work was to study the peculiarity of the expression of tau protein in the sensomotor cortex in the modeling of transient ischemia against the background of the prior sensitization of the brain antigen and immunocorrection of their effects. Materials and Methods. Studies performed were on 135 male Wistar rats. Histological, immunohistochemical, densiometric and statistical methods of investigation were used. Immunohistochemical reaction performed was according to the manufacturer's protocol with a polyclonal rabbit antibody against tau protein 1: 200 (Thermo, USA). EnVisionTM FLEX Detection System (Dako, Denmark) used was to visualize reaction products. Sections contrasted with Gyll Hematoxylin. Discussion. It has been established that sensitization with the brain antigen leads to diffuse degenerative changes in the cerebral cortex accompanied by an increase in the expression of the tau protein. Previous sensitization by the brain antigen leads to an increase in the severity of brain damage and the potentiation of the expression of the tau protein in acute circulatory disturbance. The use of immunophan provides a reduction in the expression of tau protein in the sensorimotor cortex caused by both sensitization of the brain antigen and its combination with transient disturbance of cerebral blood flow