Expression of glial fibrillar acidic protein in the sensorimotor cortex of the cerebral hemispheres in the modeling of transient ischemia against the background of previous sensitization by brain antigen and immunocorrection

• Main Authors: L. M. Yaremenko, A. N. Grabovoy, S. E. Shepelev
• Format: Article
• Language: English
• Published: Zaporozhye State Medical University 2017-12-01
• Series: Patologìâ
• Subjects: brain ischemia; GFAP; central nervous system (CNS) sensitization; immunomodulation
• Online Access: http://pat.zsmu.edu.ua/article/view/118741/113903
• ISSN: 2306-8027; 2310-1237

Aim. In order to analyze the dynamics of expression of glial fibrillar acidic protein in the sensorimotor cortex of the large hemispheres in the simulation of transient ischemia against the background of previous sensitization by brain antigen and immunocorrection. Materials and methods. The study is conducted on 185 male mature white rats from Wistar line weighing 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, immunohistochemical, morphometric and statistical methods were used. Results. Observations have shown that sensitization by the brain antigen causes neurodegenerative changes in the sensorimotor cortex and a moderate increase in the number of GFAP+-gliocytes, which is gradually increasing. The discirculatory changes that occurred with PO and BCA against the background of previous sensitization practically do not lead to changes in the number of GFAP+-cells. Against the background of sensitization by brain antigen, brain ischemia leads to an increase in the number of gliocytes that are GFAP labeled. In the affected hemisphere, their number reaches a maximum in the end of the acute period of ischemia, after which it decreases. But even in 3 months after transient vascular lesion, there are almost twice as many as in conditionally intact rats. This can be a factor that will significantly affect the function of brain regions after a vascular accident. The increase in the number of GFAP+-gliocytes in the contralateral hemisphere allows us to speak about a certain systemic response of astrocytic glia after ischemic trauma. An early reaction to increase of the number of labeled astrocytes just a day after ischemic attack suggests that some of this type of gliocytes does not expresses GFAP under normal conditions. The action of Imunofan in MEAs results in a less significant decrease in manifestations of neurodegeneration and an increase in the number of GFAP+-gliocytes. Moreover, these effects are observed both from the side of circulatory disturbance, and from the contralateral side, where immune damage is prevalent. The latter testifies to the modulation of Imunofan by the immune response in brain damage. Conclusions. Sensitization by the brain antigen causes neurodegenerative changes in the sensorimotor cortex and an increase in the number of GFAP+-astrocytes. Sensitization by brain antigen leads to the potentiation of an increase in the number of GFAP+-astrocytes in response to transient circulatory disturbances in the cerebral cortex. Immunofan significantly reduces the severity of neurodegenerative changes and the number of GFAP+-astrocytes in the cerebral cortex caused by both ischemic attack and sensitization.