Abstract
The article shows the results of a complex study of the leading index changes of the cytokine profile in patients with the brain infarction (BI) in the course of therapy with human cryopreserved cord blood serum (CCBS). Plasma levels of proinflammatory cytokines (interleukine-6 (IL-6), tumor necrosis factor-α (TNF-α)) as well as anti-inflammatory factors – IL-4, IL‑10 were tested in the blood serum of 350 patients in the mentioned medical condition on the 1st, 10th and 21st days of therapy. All patients were divided into 2 groups: the 1st one (n = 175) got undifferentiated therapy with the additional administration of acetylsalicylic acid (ASA); the 2nd one (n = 175) got the therapy of 1st group complemented by administration of 1 ml of CCBS within 10 days. Additionally there were 2 more clinical sub-groups distinguished by National Institutes of Health Stroke Scale (NIHSS) according to disease severity level: A group (n = 183) included patients in medium severity condition; B group (n = 167) comprised patients in critical condition. Plasma levels of IL-4, IL-6, IL-10 and TNF-α were specified by means of enzyme-linked immunosorbent analysis. Summing up the above-mentioned, it is certain that the imbalance in immune system functioning, represented by a simultaneous lytic level increase of both proinflammatory (IL-6, TNF-α) and anti-inflammatory (IL‑4, IL-10) cytokines, is observed shortly after the start of BI. Additional administration of CCBS in a therapeutic complex caused more considerable and more rapid stabilization of proinflammatory factor values, which were ultimately close to the control ones. This substantially influenced the course of disease and its prognosis. The research showed no accurate reduction in anti-inflammatory cytokines levels of ІL-4 and ІL-10 which indicated intensive localized inflammatory response even at the end of the acute period of disease. However, comparing the mentioned values with those of the patients who were not additionally treated with CCBS, lower value levels have to be acknowledged. It may be explained by a more efficient and incipient reduction of proinflammatory cytokines concentration in the course of disease, which in its turn results in normalization of ІL-4 and ІL-10 levels.
Highlights
The localized inflammatory response of the brain tissue within acute anoxia occurs due to rapid formation of cytokines, which are specific bioregulatory glycoproteins
Summing up the above-mentioned, it is certain that the imbalance in immune system functioning, represented by a simultaneous lytic level increase of both proinflammatory (IL-6, tumor necrosis factor-α (TNF-α)) and anti-inflammatory (IL-4, IL-10) cytokines, is observed shortly after the start of brain infarction (BI)
The levels of proinflammatory (ІL-6 and TNF-α) and antiinflammatory (ІL-4 and ІL-10) cytokines were studied in the blood serum of 350 patients in mentioned medical condition during their hospitalization on the 1st, 10th and 21st days of therapy in order to determine the degree of changes of cytokine profile in the course of BI
Summary
The localized inflammatory response of the brain tissue within acute anoxia occurs due to rapid formation of cytokines, which are specific bioregulatory glycoproteins. By their functional properties they are divided into pro- and antiinflammatory units [1, 2]. Due to its binding to the targeting membrane receptors at molecular level the signaling events are started that result in activating the transcription factors which in their turn control the activity of genes which encode the fusion of proinflammatory cytokines and cause a programmed cell death [8, 9].
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