Acute disorders of cerebral circulation are one of the leading problems of modern clinical medicine, due to their significant spread in the human population and the extremely negative impact exerted on the patient’s body. Currently available data allow us to talk about the multi-vector nature of the pathogenesis of ischemic brain damage. Within the framework of the cascade of developing pathochemical and pathophysiological processes, an essential role in the formation of ischemic stroke belongs to the inflammatory reaction occurring through the immune system’s response to cerebral tissue ischemia. One of the places of its implementation is the vessel wall located in the ischemic zone, where monocytes and neutrophils are attracted with the help of cell adhesion proteins. Complement activation plays a significant role, carried out mainly due to the C3 component or during the initialization of the mannose pathway. Activation of microglia and astrocytes plays a huge role directly in the focus of ischemia. It should be noted that in the process of activation, both microglia and astrocytes are able to acquire a pro-inflammatory or anti-inflammatory phenotype. The prevalence of the pro-inflammatory variant contributes to prolonged damage to brain tissue, while the predominance of the anti-inflammatory phenotype has a protective effect. An important role is played by a violation of the function of the blood-brain barrier, which provides an additional influx of leukocytes to the site of ischemia. In addition, individual subpopulations of T-lymphocytes penetrating through the damaged barrier also play a significant role in the organization and dynamics of the immuno-inflammatory response. The action of Th1 and Th2 cells, gamma-delta T lymphocytes, natural killer cells, as well as regulatory T lymphocytes has been most studied. The role of B-lymphocytes in the formation of a stroke focus is considered.

INTRODUCTION. It is well known that diabetes mellitus (DM) is not only one of the leading risk factors for the development of ischemic stroke (IS), but also the cause of its adverse outcomes. Along with this, with IS in people with diabetes, slow regression of cerebral edema is observed. Despite the availability of clinical recommendations for the treatment of IS and diabetes, disability and mortality in the group of patients with a combination of these diseases remains high today. Meanwhile, since the 2000s. A number of studies have demonstrated the benefits of using Glibenclamide in the treatment of cerebral edema associated with IS. However, we did not find any studies in the available literature that assessed its effectiveness in treating stroke in people with diabetes. AIM . Improving the effectiveness of treatment of patients with type II diabetes mellitus undergoing ischemic stroke. MATERIALS AND METHODS. An assessment of clinical and functional outcomes, as well as changes in the size of cerebral ischemic zones based on magnetic resonance imaging data, was conducted in 67 patients with type 2 diabetes during the acute phase of non-lacunar IS. Glibenclamide was used in the treatment of the main group of patients. Stroke treatment in the comparison group was conducted in accordance with generally accepted clinical guidelines and standards. RESULTS. In a cohort of patients with type 2 diabetes mellitus treated with glibenclamide, the median change in the severity of neurological deficit according to the National Institutes of Health Stroke Scale (NIHSS) by the end of treatment was 5 points; the Rivermead Mobility Index reached 9 points; the Barthel Activity of Daily Living Index increased to 75 points; the relative number of functionally independent patients was 30.8 %. In the standard treatment group, the stroke severity according to the NIHSS scale decreased by only 2 points; the Rivermead Mobility Index reached only 7 points; the Barthel Activity of Daily Living level increased to only 55 points; the relative number of functionally independent patients reached only 17.1 %. The size of ischemic brain damage according to MRI results in the glibenclamide group decreased by 67.1 %, in the standard treatment group – by 11.6%. CONCLUSION . The differences revealed between the groups indicate the ability of Glibenclamide to exert a protective effect in ischemic injury and improve the outcomes of the acute period of non-lacunar ischemic stroke in individuals with type 2 diabetes.

Background. Ischemic stroke (IS) in patients with type 2 diabetes mellitus (DM 2) is characterized by a more severe course and worse functional outcomes compared to individuals without diabetes, which increases the number of patients disabled by the end of hospitalization. Predicting the outcome of stroke upon admission to hospital can help optimize treatment, diagnostic and rehabilitation measures and improve the quality of treatment. The use of laboratory biomarkers (LBM) in predicting the outcome of IS is a promising area of modern medicine. Objective. To create a prognostic model for the outcome of non-lacunar ischemic stroke (NlIS) in patients with DM 2 based on the LBM study. Design and methods. We studied the serum concentrations of 78 LBM in 55 patients with DM 2 admitted to the hospital due to the development of NlI S. Machine learning (ML) was used to search for a relationship between LBM levels at the time of patient admission to hospital and outcomes of the acute period of stroke. Results. We established the threshold concentrations of interleukin (IL)-13 (3,605 pg/mL), IL-6 (1,47 pg/mL), apolipoprotein CII (1516000000,0 ng/mL), soluble IL-4 receptor (581,912 pg/mL) and syndecan 4 (26,785 ng/mL) that determine the functional outcome of IS, as well as the threshold values of the alpha subunit of the soluble IL-2 receptor (480,802 pg/mL), IL-21 (1,024 pg/mL), protein 15 containing a disintegrin and metalloproteinase domain (3076,733 ng/mL), soluble vascular endothelial growth factor receptor 2 (16,300,003 pg/mL) that determine the neurological outcome of IS in patients with DM 2. Models for predicting the functional and neurological outcome of IS in patients with DM 2 are proposed. Conclusion. LBM research can be a useful auxiliary tool for predicting the outcomes of NlIS in patients with DM 2, which provides opportunities for implementing a personalized approach to the management of these patients and improving the quality of their treatment.