scholarly journals EXPERIMENTAL INVESTIGATION ON CARBACETAM INFLUENCE ON HYPOTHALAMUS TISSUE IN BRAIN INJURY

2018 ◽  
Vol 14 (1-2) ◽  
pp. 11-17
Author(s):  
S.V. Ziablytsev ◽  
T.I. Panova ◽  
O.O. Starodubska ◽  
O.O. Dyadik
Keyword(s):  
Brain Injury ◽  
Physiological Saline ◽  
Neuroendocrine Cells ◽  
Nerve Tissue ◽  
Male Rats ◽  
Control Group ◽  
S 100 ◽  
Hypothalamic Tissue ◽  
Hematoxylin And Eosin ◽  
The Brain

Relevance. A key role in the pathogenesis of the brain injury is played by destructive changes in the hypothalamus neuroendocrine cells. For the correction of such disorders, promising is carbacetam, which has antihypoxic, anti-edema and anti-shock effects. Objective: to investigate the effect of carbacetam on the processes of neurodegeneration in the paraventricular and supraoptical nuclei of the hypothalamus in the experimental brain injury. Material and methods. Brain injury were modeled on the V.M. Elskyy &S.V. Ziablitsev model on white non-breeding male rats weighing 200±10 g. Experimental animals (n=10) received intraabdominal injection of carbacetam at a dose of 5 mg/kg in 1 ml of physiological saline during the seven days after injury. In the control group (n=10), 1 ml of physiological saline was injected. Hypothalamic tissue microparticles performed a morphological and immunohistochemical evaluation of neurodegenerative changes when stained with hematoxylin and eosin and immunohistochemically to detect NSE, S-100 and GFAP neuromarkers. Results. Carbacetam reduced the degenerative processes in the nervous tissue of the paraventricular and supraoptical nuclei of the hypothalamus, which was manifested by the restoration of normal morphological features, in contrast to rats that did not receive the drug. Immunohistochemically, GFAP and S-100 glial markers exhibited reduced, reflecting a reduction in degenerative changes in the nerve tissue. Expressions of the neurons marker NSE increased, reflecting high metabolic activity of the neurons. Conclusions. Revealed changes in the expression of markers of neurons and glia showed a restoration of normal neuronal activity due to the introduction of carbacetam.

scholarly journals EXPERIMENTAL INVESTIGATION ON CARBACETAM INFLUENCE ON HYPOTHALAMUS TISSUE IN BRAIN INJURY

2018 ◽  
Vol 14 (1-2) ◽  
pp. 11-17 ◽  
Author(s):  
S.V. Ziablytsev ◽  
T.I. Panova ◽  
O.O. Starodubska ◽  
O.O. Dyadik
Keyword(s):  
Brain Injury ◽  
Physiological Saline ◽  
Neuroendocrine Cells ◽  
Nerve Tissue ◽  
Male Rats ◽  
Control Group ◽  
S 100 ◽  
Hypothalamic Tissue ◽  
Hematoxylin And Eosin ◽  
The Brain

Relevance. A key role in the pathogenesis of the brain injury is played by destructive changes in the hypothalamus neuroendocrine cells. For the correction of such disorders, promising is carbacetam, which has antihypoxic, anti-edema and anti-shock effects. Objective: to investigate the effect of carbacetam on the processes of neurodegeneration in the paraventricular and supraoptical nuclei of the hypothalamus in the experimental brain injury. Material and methods. Brain injury were modeled on the V.M. Elskyy &S.V. Ziablitsev model on white non-breeding male rats weighing 200±10 g. Experimental animals (n=10) received intraabdominal injection of carbacetam at a dose of 5 mg/kg in 1 ml of physiological saline during the seven days after injury. In the control group (n=10), 1 ml of physiological saline was injected. Hypothalamic tissue microparticles performed a morphological and immunohistochemical evaluation of neurodegenerative changes when stained with hematoxylin and eosin and immunohistochemically to detect NSE, S-100 and GFAP neuromarkers. Results. Carbacetam reduced the degenerative processes in the nervous tissue of the paraventricular and supraoptical nuclei of the hypothalamus, which was manifested by the restoration of normal morphological features, in contrast to rats that did not receive the drug. Immunohistochemically, GFAP and S-100 glial markers exhibited reduced, reflecting a reduction in degenerative changes in the nerve tissue. Expressions of the neurons marker NSE increased, reflecting high metabolic activity of the neurons. Conclusions. Revealed changes in the expression of markers of neurons and glia showed a restoration of normal neuronal activity due to the introduction of carbacetam.

scholarly journals NEURODESTRUCTION OF HYPOTHALAMIC NUCLEI IN BRAIN INJURY. EFFECT OF CARBACETAM

2018 ◽  
Vol 13 (3-4) ◽  
pp. 3-9
Author(s):  
S.V. Ziablitsev ◽  
T.I. Panova ◽  
O.O. Starodubska
Keyword(s):  
Brain Injury ◽  
Nervous Tissue ◽  
Free Fall ◽  
Benzodiazepine Receptor ◽  
Expression Level ◽  
Male Rats ◽  
Control Group ◽  
S 100 ◽  
The Brain ◽  
Supraoptic Nuclei

Relevance. A key role in the pathogenesis of brain injury (BI) is played by destructive changes in the neural tissue of the brain, which consist in damage to neurons and glial cells. To date, various drugs are being intensively developed and studied, which are considered in the perspective of correction and restoration of the functional state of the brain. These substances include the neuroprotector carbacetam, an modulator of the GABA-benzodiazepine receptor complex, a derivative of the alkaloid β-carboline. Objectie. To investigate the effect of carbacetam on neurodestruction processes in the paraventricular and supraoptic nuclei of the hypothalamus in experimental BI. Material and methods. The study was carried out on 20 white non-native male rats weighing 200±10 g. To simulate the BI, rats were subjected to one stroke along the cranial vault with a free-fall load according to the V.N. Yelskyy and S.V. Ziablitsev method (2008). The energy of impact was 0.52 J, the lethality for the first 5 days after injury was 84%. In the control group (n=10) 1 ml of saline was injected intraperitoneally once daily for 10 days after injury. Animals of the experimental group (n=10) received intraperitoneally injections of carbacetam at a dose of 5 mg/kg in 1 ml of saline according to the same scheme. After the experiment was over, the animals were decapitated with the removal of the brain, from which histological preparations were made with a microtome after appropriate histological treatment. Some sections were stained with hematoxylin and eosin, others were immunohistochemically reacted with antibodies against neuronmarkers proteins NSE, S-100 and GFAP. Results. Carbacetam influenced the decrease of degenerative processes in the nervous tissue of the paraventricular and supraoptic nuclei of the hypothalamus. Neurons of animals with BI that received carbacetam, were characterized by the restoration of normal morphological features in contrast to rats not receiving the drug. Immunohistochemical study of brain neuromarkers confirmed the restoration of the functions of neurons and astrocytes in the investigated parts of the rat's hypothalamus after the administration of carbacetam. There was a decrease in the expression level of glial markers GFAP and S-100, which illustrated the decrease in degenerative changes in the nervous tissue. While the expression level of the neuron marker NSE grew, this demonstrated the high metabolic activity of nerve cells. Changes in the expression of markers of neurons and glia indicated a restoration of normal neuronal activity under the action of carbacetam. Conclusion. Further investigation of the effects of carbacetam seems promising in terms of the restoration of neuronal function at BI.

scholarly journals Experimental Brain Injury Induced by Acute Hypobaric Hypoxia Stimulates Changes in mRNA Expression and Stress Marker Status

2021 ◽  
Vol 8 (10) ◽  
pp. 242-247
Author(s):  
Muhammad Shoaib Tahir ◽  
Maged Almezgagi ◽  
Yu Zhang
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Mrna Expression ◽  
Hypobaric Hypoxia ◽  
Male Rats ◽  
Control Group ◽  
Dependent Manner ◽  
Acute Hypobaric Hypoxia ◽  
Time Duration ◽  
The Brain

The present study was proposed to investigate the brain injury under acute hypobaric hypoxia following alteration in mRNA expression and stress markers in a time-dependent manner. SD clean graded male rats were randomly divided into four groups for this experimental brain injury, the control group at Xining (altitude, 2270m) and hypoxia treatment groups with different time exposure day1, day2, and day3 at (altitude, 7000m) in a hypobaric chamber. After day3 exposure, the brain tissues were collected. The level of mRNA expression of VEGF and HIF1-α was assessed using qRT-PCR. The oxidative stress level of superoxide dismutase (SOD) and malondialdehyde (MDA) were determined with commercial kits. AHH with time duration significantly increased the MDA level and decreased in the activity of SOD was seen in all hypoxia treated groups as compared to the control (P< 0.001). The mRNA expression level of HIF1-α and VEGF in day1, day2, and day3 AHH groups was markedly raised when it is compared to control (P< 0.05). Ultimately, in conclusion, such results indicate that AHH stimulates oxidative stress induces brain damage in rats. Keywords: Acute hypobaric hypoxia, Brain injury, HIF-1α, Oxidative stress.

Chronic immobilization stress induces anxiety-related behaviors and affects brain essential minerals in male rats

2020 ◽  
pp. 1-8
Author(s):  
Zafer Sahin ◽  
Alpaslan Ozkurkculer ◽  
Omer Faruk Kalkan ◽  
Ahmet Ozkaya ◽  
Aynur Koc ◽  
...  
Keyword(s):  
Immobilization Stress ◽  
Central Area ◽  
Essential Elements ◽  
Male Rats ◽  
Control Group ◽  
Male Wistar Rats ◽  
Swimming Test ◽  
The Brain ◽  
Center Area ◽  
Chronic Immobilization Stress

Abstract. Alterations of essential elements in the brain are associated with the pathophysiology of many neuropsychiatric disorders. It is known that chronic/overwhelming stress may cause some anxiety and/or depression. We aimed to investigate the effects of two different chronic immobilization stress protocols on anxiety-related behaviors and brain minerals. Adult male Wistar rats were divided into 3 groups as follows ( n = 10/group): control, immobilization stress-1 (45 minutes daily for 7-day) and immobilization stress-2 (45 minutes twice a day for 7-day). Stress-related behaviors were evaluated by open field test and forced swimming test. In the immobilization stress-1 and immobilization stress-2 groups, percentage of time spent in the central area (6.38 ± 0.41% and 6.28 ± 1.03% respectively, p < 0.05) and rearing frequency (2.75 ± 0.41 and 3.85 ± 0.46, p < 0.01 and p < 0.05, respectively) were lower, latency to center area (49.11 ± 5.87 s and 44.92 ± 8.04 s, p < 0.01 and p < 0.01, respectively), were higher than the control group (8.65 ± 0.49%, 5.37 ± 0.44 and 15.3 ± 3.32 s, respectively). In the immobilization stress-1 group, zinc (12.65 ± 0.1 ppm, p < 0.001), magnesium (170.4 ± 1.7 ppm, p < 0.005) and phosphate (2.76 ± 0.1 ppm, p < 0.05) levels were lower than the control group (13.87 ± 0.16 ppm, 179.31 ± 1.87 ppm and 3.11 ± 0.06 ppm, respectively). In the immobilization stress-2 group, magnesium (171.56 ± 1.87 ppm, p < 0.05), phosphate (2.44 ± 0.07 ppm, p < 0.001) levels were lower, and manganese (373.68 ± 5.76 ppb, p < 0.001) and copper (2.79 ± 0.15 ppm, p < 0.05) levels were higher than the control group (179.31 ± 1.87 ppm, 3.11 ± 0.06 ppm, 327.25 ± 8.35 ppb and 2.45 ± 0.05 ppm, respectively). Our results indicated that 7-day chronic immobilization stress increased anxiety-related behaviors in both stress groups. Zinc, magnesium, phosphate, copper and manganese levels were affected in the brain.

scholarly journals The Effect of Herniarin on Spatial Working Memory, Pain Threshold, and Oxidative Stress in Ischemic Hypoperfusion Model in Rats

2021 ◽  
Vol 7 (1) ◽  
pp. 42-50
Author(s):  
Zahra Nazari Barchestani ◽  
◽  
Maryam Rafieirad ◽  
Keyword(s):  
Oxidative Stress ◽  
Pain Threshold ◽  
Male Rats ◽  
Control Group ◽  
Tail Flick ◽  
Pain Thresholds ◽  
Ischemic Group ◽  
Significant Difference ◽  
The Brain ◽  
And Oxidative Stress

Background: Ischemia causes severe neuronal damage and induces oxidative stress, memory impairment, and reduces pain threshold. Herniarin is a powerful antioxidant. Objectives: This study aimed to evaluate the effect of herniarin on memory, pain, and oxidative stress in an ischemia model in male rats. Materials & Methods: In this study, 50 male rats were divided into 5 groups of control, sham, ischemic, and two other ischemic groups, which received herniarin at doses of 150 and 300 mg/kg by gavage for 14 days. Behavioral tests were performed by shuttle box, and Y-maze and pain tests were performed by Tail-Flick test. Then, the rats’ brains were extracted to evaluate lipid peroxidation and measure the levels of thiol and Glutathione Peroxidase (GPX) in the hippocampus and striatum tissues. The results were expressed as Mean±SEM and then analyzed using suitable statistical methods of ANOVA and least significant difference post-hoc test in SPSS V. 20. Results: Herniarin significantly increased the avoidance memory, spatial memory, and pain thresholds of ischemic rats at different concentrations (P<0.001). Besides, the amount of malondialdehyde (MDA) and thiol in the ischemic group increased significantly in comparison to the control group (P<0.001). Also, in the ischemic group, GPX (P<0.001) significantly decreased. Decreased MDA (P<0.001) and thiol (P<0.001) and increased GPX levels were observed with herniarin administration (P<0.01). Conclusion: According to this study’s results, herniarin can remove free radicals and oxidant substances from the brain. Thus, it improves memory and pain thresholds in the brain hypoperfusion ischemia model.

Comorbidity: Chronic neurogenic pain affects malignant growth and changes balance of neurosteroids in brain of rats.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e23516-e23516
Author(s):  
Yulia A. Pogorelova ◽  
Ekaterina I. Surikova ◽  
Elena M. Frantsiyants ◽  
Valeria A. Bandovkina ◽  
Irina V. Kaplieva ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Subclavian Vein ◽  
Tumor Development ◽  
Stress Factors ◽  
Male Rats ◽  
Control Group ◽  
Malignant Growth ◽  
Neurogenic Pain ◽  
Pulmonary Tissue ◽  
The Brain

e23516 Background: Sex steroids in the brain regulate neurogenesis and the body's response to stress. Chronic neurogenic pain (CNP) and the tumor growth are stress factors that often accompany each other. The purpose of the study was to analyze levels of sex steroid hormones in white matter of the brain of rats with tumor development in presence of CNP. Methods: The study included white outbred male rats (n = 74). In the main groups, a CNP model was created by bilateral sciatic nerve ligation, and after 45 days, M1 sarcoma was transplanted subcutaneously (n = 11) or into the subclavian vein (n = 11). Two comparison groups (each n = 13) included sham operated animals with M1 sarcoma transplanted subcutaneously or into the subclavian vein. Control groups (each n = 13) included animals with CNP or sham operated rats. Levels of testosterone (T), estrone (E1), estradiol (E2), estriol (E3) and progesterone (P4) were measured by ELISA (Cusabio, China) in the brain tissues obtained on day 21 of the tumor growth. Results: Tumors transplanted subcutaneously with and without CNP grew in 100% of animals. Tumor volumes were 1.5 times (p<0.05) greater in animals with CNP, compared with rats without CNP, while the survival in the groups was similar. Levels of all studied hormones, except for E1, in the brain tissue in subcutaneous sarcoma growth were lower in presence of CNP than without it: T and E3–on average by 1.4 times (p<0.05), E2 and P4–by 3.5 times (p<0.05). In rats with intravenous transplantation of M1, tumor nodes in the lungs were registered only in rats with CNP, and the survival of animals was 36 days shorter (p<0.05) than in rats of the corresponding control group. Such specificity of selective neoplastic growth in the pulmonary tissue was combined with lower cerebral T and E3 levels than in the corresponding control–on average by 1.4 times (p<0.05), E2–by 7.2 times, and higher levels of E1–by 1.3 (p<0.05) and P4–by 2.0 times, compared to animals which did not develop the neoplastic process in the lungs without pain. Conclusions: The presence of CNP stimulates the growth of M1 sarcoma in standard subcutaneous inoculation and allows the development of tumors in the lung in intravenous inoculation. The specificity of malignant growth in presence of CNP is accompanied by changes in the brain levels of neurosteroids in rats.

PROLONGED BAKTERIOPHAGAL INFECTION OF GUT MICROBIOTA REDUCES THE EXPRESSION OF ALPHA-SYNUCLEIN IN THE RAT PANETH CELLS

2020 ◽  
pp. 60-65
Author(s):  
Татьяна Николаевна Сергеева ◽  
Владимир Николаевич Николенко ◽  
Юлия Николаевна Кузнецова ◽  
Валерий Георгиевич Сергеев
Keyword(s):  
Gut Microbiota ◽  
Experimental Studies ◽  
Physiological Saline ◽  
Alpha Synuclein ◽  
Paneth Cells ◽  
Male Rats ◽  
Control Group ◽  
Human Pathogens ◽  
Bacteriophage Infection ◽  
Intestinal Dysbiosis

Цель - исследовать интенсивность экспрессии белка альфа-синуклеина клетками Панета у крыс в норме и условиях длительного бактериофагального инфицирования микробиоты. Материал и методы. Экспериментальные исследования проведены на 12 половозрелых крысах-самцах линии Вистар массой 280-320 г. Крысам основной группы (n=7) еженедельно на протяжении 12 нед ректально вводили 0,5 мл раствора, содержащего смесь бактериофагов против 14 патогенов человека (Microgen, Россия). Однократная доза вводимой бактериофагальной смеси содержала 0,5×10ед./мл каждого фага. Животные контрольной группы (n=5) получали по аналогичной схеме 0,5 мл стерильного изотонического раствора натрия хлорида. После интракардиальной перфузии отбирали фрагменты проксимального отдела подвздошной кишки на уровне 1-3 см выше илеоцекального соединения. Серийные криостатные срезы кишечника использовали для окрашивания гематоксилином - эозином и выявления иммунопозитивного альфа-синуклеина при помощи моноклональных мышиных антител (Sigma-Aldrich, USA) и коммерческого набора, содержащего авидин-биотин-пероксидазный комплекс (АBC Elite; Vector Laboratories, Burlingame, CA). Результаты. Длительное бактериофагальное инфицирование приводило к значимому снижению относительно контроля количества клеток, иммунопозитивных к альфа-синуклеину. В клетках Панета значимо снижались площади, занимаемые иммунореактивным продуктом к альфа-синуклеину и ацидофильными гранулами. Выводы. В апикальных частях клеток Панета, в области локализации ацидофильных гранул детектируется иммунопозитивный альфа-синуклеин. Дисбиоз кишечника, вызываемый бактериофагальным инфицированием микробиоты, приводит к гранулярному истощению клеток Панета и снижению экспрессии в них иммунореактивного альфа-синуклеина, что свидетельствует о его вовлеченности в механизмы экскреции. Objective - to investigate the intensity of the alpha - synuclein expression by Paneth cells of rat in normal conditions and prolonged bacteriophagal infection of gut microbiota. Material and methods. Experimental studies were performed on 12 adult Wistar male rats weighting 280-320 g. The rats of the main group (n=7) received rectally a 0,5 ml of solution containing a mixture of bacteriophages directed against 14 human pathogens (Microgen, Russia). The solution was introduced weekly for a period of 12 weeks. Each dose of bacteriophagal mixture contained 0,5×10 units/ml of each phage. Animals of the control group (n=5) received 0,5 ml of sterile physiological saline according to the same scheme. After transcardial perfusion, specimens of proximal portion of ileum 1-2 cm upstream the ileocecal junction were obtained. Serial cryostat sections were used for hematoxylin and eosin staining and for detection of immunopositive alpha-synuclein by monoclonal mouse antibodies (Sigma-Aldrich, USA) and commercially available kit containing avidin-biotin-peroxidase complex (АBC Elite; Vector Laboratories, Burlingame, CA). Results. Prolonged bacteriophage infection led to a significant decrease in the number of alpha-synuclein immunopositive cells compared with control. The area of Paneth cells occupied by the alpha synuclein-immunoreactive product and acidophilic granules significantly reduced. Conclusions. Immunopositive alpha-synuclein was detected in the apical parts of Paneth cells, in the area of acidophilic granules localization. The intestinal dysbiosis caused by bacteriophage infection of microbiota led to granular depletion of Paneth cells and a decrease in the expression of immunoreactive alphasynuclein in them, which indicates its involvement in excretion mechanisms.

Abstract WP288: Inter-Alpha Inhibitor Proteins Reduce the Presence of Neutrophils and Matrix Metalloproteinase-9 Positive Neutrophils in Damaged Brain Regions of Neonates with Hypoxic-Ischemic (HI) Brain Injury

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Adriel Barrios-Anderson ◽  
Xiaodi Chen ◽  
Yow-Pin Lim ◽  
Barbara S Stonestreet
Keyword(s):  
Brain Injury ◽  
Corpus Callosum ◽  
Matrix Metalloproteinase ◽  
Right Hemisphere ◽  
Brain Regions ◽  
Matrix Metalloproteinase 9 ◽  
Male Rats ◽  
Control Group ◽  
Neonatal Rats ◽  
Metalloproteinase 9

Introduction: Inter-alpha inhibitor proteins (IAIPs) are immunomodulatory proteins that play a significant anti-inflammatory role in hypoxic ischemic (HI) brain injury. We have shown that administering IAIPs after HI improves histopathological brain injury, brain weight, and behavioral outcomes in neonatal rats. Neutrophils are specialized leukocytes known to infiltrate the brain parenchyma and exacerbate neuronal injury after HI. One molecular mechanism by which neutrophils exert damage on the blood-brain barrier (BBB) and brain tissue after ischemia is by the release of matrix metalloproteinase-9 (MMP9), an enzyme that breaks down the extracellular matrices of surrounding cells. Objective: To determine the effect of IAIPs on neutrophil infiltration and release of MMP9 in neonatal rats after HI. Methods: The Vannucci model was used to induce neonatal HI in postnatal day 7 rats that were assigned to a Non-ischemic sham-control group (Sham, n=12), right-sided carotid ligation with exposure to hypoxia (8% oxygen for 90 min) treated with placebo group (PL-HI, n=17), or an IAIP treated group (IAIP-HI, n=17). Rat sex was recorded. IAIP (30 mg/kg) or PL was given intraperitoneally at 0, 24 and 48 h after HI. We removed the rat brain after 72h and performed immunohistochemistry using MPO (neutrophil selective) and MMP9 fluorescent markers. We performed stereological analyses with the StereoInvestigator 10.0 Fractionator probe without knowledge of group assignment to quantify neutrophils and MMP9 positive cells present within the right hemisphere, cortex, corpus callosum, and hippocampus. Results: MPO positive cells were significantly reduced in male IAIP treated rats compared with PL-HI in the overall damaged hemisphere (p<0.01) and the corpus callosum (p<0.05). Further, we observed MPO and MMP9 co-localization, and IAIP treatment reduced the presence of MMP9 positive neutrophils in the cortex of male rats compared to placebo (P<0.05).

Fetal electrocardiographic monitoring during labor in relation to cord blood levels of the brain-injury marker protein S-100

2008 ◽  
Vol 36 (2) ◽  
Author(s):  
Andrea Stuart ◽  
Linda Edvinsson ◽  
Karin Källen ◽  
Per Olofsson ◽  
Charlotte Hellsten ◽  
...  
Keyword(s):  
Brain Injury ◽  
Cord Blood ◽  
Protein S ◽  
Blood Levels ◽  
Marker Protein ◽  
Electrocardiographic Monitoring ◽  
S 100 ◽  
The Brain

scholarly journals THE IMPORTANCE OF CENTRAL CHOLINERGIC SYSTEMS ACTIVATION IN TRAUMATIC BRAIN INJURY

2020 ◽  
Vol 16 (3) ◽  
pp. 3-8
Author(s):  
S.V. Ziablitsev ◽  
S.O. Khudoley
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neurological Deficit ◽  
Physiological Saline ◽  
Neurological Deficits ◽  
Control Group ◽  
Post Traumatic Stress ◽  
Acute Period ◽  
Cholinergic Systems ◽  
Release Of Acetylcholine

Relevance. It is known that in traumatic brain injury (TBI), the activity of the central cholinergic systems (CChS) is inhibited, the release of acetylcholine and the expression of cholinergic receptors decrease. The restoration of cholinoreactivity is an urgent area of research and a possible therapeutic direction. Objective – to determine the effect of CChS activation on mortality, neurological disorders, and the activity of the pituitary-corticoadrenal system (PCAS) in the acute period of TBI. Material and methods. TBI was simulated with a free load’s fall on a fixed animal head. To activate the CChS, rats were injected with choline alfoscerate (gliatilin, 6 mg/kg) before the injury, physiological saline was injected in the control group. Neurological deficits were assessed using the 100-point Todd scale. In blood plasma, 3, 24, 48, and 72 hours after injury, the content of adrenocorticotropic hormone and corticosterone was determined by the enzyme immunoassay method (DSL; USA). The results were statistically processed using the SPSS 11.0, MedStat, MedCalc software. Results. Mortality in the control group was 25.0%, in the group with activation of the CChS there were no lethal cases (p<0.05). The neurological deficit in the group with CChS activation was significantly less pronounced compared to the control at all periods of observation. The hormone content had a similar dynamics: it reached a maximum after 24 hours and recovered after 72 hours, however, upon activation of the CChS, the increase was 1.4-1.5 times less (p<0.05). Thus, the use of choline alfoscerate for modeling the CChS activity led to a decrease in mortality and neurological deficit in the acute period of TBI, which was accompanied by a stabilizing PCAS function. Conclusion. The important role of CChS in the implementation of post-traumatic stress reaction of PCAS, as well as the possibility of its pharmacological correction with choline alfoscerate, was established.

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