Експресія білка NF-L в сенсомоторній корі при моделюванні транзиторної ішемії на тлі сенсибілізації мозковим ан-тигеном та імунокорекції змін, що виникли.

Abstract

Aim. To study the levels of NFР-L protein expression in the sensorimotor cortex of rats in the simulation of transient ischemia against the background of sensitization by the brain antigen and immunocorrection of the resulting changes by imunofan. Materials and methods. The study was conducted on 185 male mature white rats from Wistar line weighted 260–290 g, in which the damage of the brain was modulated. The brain for study was taken on the 1st, 3rd, 10th, 30th and 90th days after the start of the experiment. The histological, immunehistochemical, morphometric and statistical methods were used. Results. Observations have shown that sensitization with the brain antigen causes diffuse degenerative changes in the cerebral cortex and a decrease in NFP-L expression. This background leads to an increase in the severity of brain damage in acute circulatory disturbances compared with when no sensitization was performed. After transient ischemic attack, the recovery period was significantly less than in the absence of sensitization, rounded corpuscles with a relatively high level of expression of NFР-L, which we qualified as nerve growth flasks (cones). This allows us to say that sensitization by the brain antigen delays the regeneration of nerve fibers, which is an important component of compensatory-recovery processes in the cerebral cortex after ischemic attack. Imunofan under the conditions of modeling of combined immune-vascular lesions of the brain had protective properties and reduced the severity of the decrease in NFР-L expression. We attribute these effects of imunofan, especially in the recovery period after brain damage in the first place, to its immunomodulatory effect which is confirmed by comparing the dynamics of the restoration of NFР-L expression in the affected and contralateral hemispheres, where the latter experienced immune damage in the absence of ischemia. Conclusions. Sensitization by the brain antigen leads to diffuse degenerative changes in the cerebral cortex, which are accompanied by a decrease in the expression of NFР-L. Previous sensitization by brain antigen in acute impairment of cerebral circulation leads to increased severity of brain damage and decreased expression of NFР-L, slows and changes the dynamics of its recovery. The effect of immunophan use is to reduce changes in NFР-L expression in the sensorimotor cortex caused by both sensitization with the brain antigen and in combination with transient impairment of cerebral blood flow.