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Oxytocin is synthesized in endothelial cells of the cardiovascular system and exerts its effects by oxytocin receptors. The effect of oxytocin on vascular tone, blood pressure, vascular growth and remodeling, as well as participation in cardiovascular regulation has been proven. The positive effect of oxytocin on infarct size and recovery of contractile function in reperfusion is well studied. It should be noted that the mechanisms of this cardioprotective effect have not yet been studied. Research evidence suggests that oxytocin therapy significantly improves cardiac function, reduces inflammation and apoptosis, and improves scar vascularization. Oxytocin stimulates the transformation of stem cells into clones of cardiomyocytes. Oxytocin promotes angiogenesis by stimulating the formation of endothelial and smooth muscle cells. Increased consumption of glucose by cardiomyocytes, inhibition of cardiomyocyte hypertrophy, and a decrease in oxidative stress are the reasons for the positive effects of oxytocin. Oxytocin reduces inflammation, improves cardiovascular and metabolic function. This is the manifestation of the cardioprotective effect of oxytocin. Potential treatment of cardiovascular diseases with oxytocin is possible due to the pleiotropic nature of oxytocin effects. This review indicates the likely mechanisms of oxytocin action at the cellular level that are involved in cardioprotection.

The rapidly accumulating information about the new coronavirus infection and the ambiguous results obtained by various authors necessitate further research aiming at prevention and treatment of this disease At the moment, there is convincing evidence that the pathogen affects not only the respiratory but also the central nervous system (CNS) The aim of the study is to provide an insight into the molecular mechanisms underlying the damage to the CNS caused by the new coronavirus SARS-CoV-2 Results By analyzing the literature, we provide evidence that the brain is targeted by this virus SARS-CoV-2 enters the body with the help of the target proteins: angiotensin-converting enzyme 2 (ACE2) and associated serine protease TMPRSS2 of the nasal epithelium Brain damage develops before the onset of pulmonary symptoms The virus spreads through the brain tissue into the piriform cortex, basal ganglia, midbrain, and hypothalamus Later, the substantia nigra of the midbrain, amygdala, hippocampus, and cerebellum become affected Massive death of neurons, astrogliosis and activation of microglia develop at the next stage of the disease By day 4, an excessive production of proinflammatory cytokines in the brain, local neuroinflammation, breakdown of the blood-brain barrier, and impaired neuroplasticity are detected These changes imply the involvement of a vascular component driven by excessive activity of matrix metalloproteinases, mediated by CD147 The main players in the pathogenesis of COVID-19 in the brain are products of angiotensin II (AT II) metabolism, largely angiotensin 1-7 (AT 1-7) and angiotensin IV (AT IV) There are conflicting data regarding their role in damage to the CNS in various diseases, including the coronavirus infection The second participant in the pathogenesis of brain damage in COVID-19 is CD147 -- the inducer of extracellular matrix metalloproteinases This molecule is expressed on the endothelial cells of cerebral microvessels, as well as on leukocytes present in the brain during neuroinflammation The CD147 molecule plays a significant role in maintaining the structural and functional integrity of the blood-brain barrier by controlling the basal membrane permeability and by mediating the astrocyte-endothelial interactions Via the above mechanisms, an exposure to SARS-CoV-2 leads to direct damage to the neurovascular unit of the brain [ABSTRACT FROM AUTHOR] Copyright of Medical Technologies in Medicine / Sovremennye Tehnologii v Medicine is the property of Sovremennye Tehnologii v Medicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission However, users may print, download, or email articles for individual use This abstract may be abridged No warranty is given about the accuracy of the copy Users should refer to the original published version of the material for the full abstract (Copyright applies to all Abstracts )

Autistic spectrum disorders (ASD), including autism, constitute a wide range of states and are associated with deficit to social communications, limited interests, and stereotypical behavior. The development of translational medicine and personalized approaches to the treatment of ASD combine the efforts of clinicians and basic scientists and push the direction of studies towards the molecular and genetic mechanisms of developmental disorders and the search for new marker molecules for targeted correction of these states, which are impossible without use of models of ASD in animals, especially rodents. This review describes the key genetic and pharmacological models of ASD in rodents which are actively utilized in experimental studies, along with the most important behavioral tests for assessing deficits in social behavior, stereotypy, and autism-like states in experimental animals.

A common feature of neurodegenerative disorders, in particular Alzheimer's disease (AD), is a chronic neuroinflammation associated with aberrant neuroplasticity. Development of neuroinflammation affects efficacy of stem and progenitor cells proliferation, differentiation, migration, and integration of newborn cells into neural circuitry. However, precise mechanisms of neurogenesis alterations in neuroinflammation are not clear yet. It is well established that expression of NLRP3 inflammasomes in glial cells marks neuroinflammatory events, but less is known about contribution of NLRP3 to deregulation of neurogenesis within neurogenic niches and whether neural stem cells (NSCs), neural progenitor cells (NPCs) or immature neuroblasts may express inflammasomes in (patho)physiological conditions. Thus, we studied alterations of neurogenesis in rats with the AD model (intra-hippocampal injection of Aβ1-42). We found that in Aβ-affected brain, number of CD133+ cells was elevated after spatial training in the Morris water maze. The number of PSA-NCAM+ neuroblasts diminished by Aβ injection was completely restored by subsequent spatial learning. Spatial training leads to elevated expression of NLRP3 inflammasomes in the SGZ (subgranular zones): CD133+ and PSA-NCAM+ cells started to express NLRP3 in sham-operated, but not AD rats. Taken together, our data suggest that expression of NLRP3 inflammasomes in CD133+ and PSA-NCAM+ cells may contribute to stimulation of adult neurogenesis in physiological conditions, whereas Alzheimer's type neurodegeneration abolishes stimuli-induced overexpression of NLRP3 within the SGZ neurogenic niche.

We studied in vitro development of brain progenitor cells isolated from healthy 7-9-month-old Wistar rats and rats with experimental Alzheimer's disease kept under standard conditions and in enriched (multistimulus) environment in vivo. Progenitor cells from healthy animals more rapidly formed neurospheres. Considerable changes at the early stages of in vitro development of brain progenitor cells were observed in both groups kept in enriched environment.

The purpose of the study was to develop a battery of tests to study social and cognitive impairments for behavioral phenotyping of aging experimental animals with physiological neurodegeneration. Object of the study were outbred CD1 mice in the following groups: 1st group - 12-month old male mice (physiological aging); 2nd group - 2-month old male mice (control group). Social recognition test, elevated plus maze test (EPM), open field test, light-dark box test, and Fear conditioning protocol were used to estimate the neurological status of experimental animals. We found that aging male mice in a contrast to young ones have demonstrated lower social interest to female mice in the social recognition task. EPM and light-dark box tests showed increased level of anxiety in the group of aged mice comparing to the control group. Fear conditioning protocol revealed impairment of associative learning and memory in the group of aged mice, particularly, fear memory consolidation was dramatically suppressed. Analysis of behavioral factors, social interactions and anxiety level in the experimental mice has confirmed age-related neurodegeneration in the 1st group. We found that the most informative approach to identifying neurological impairments in aging mice (social interaction deficit, limitation of interests, increased level of anxiety) should be based on the open field test light-dark box test, and Fear conditioning protocol. Such combination allows obtaining new data on behavioral alterations in the age-associated of neurodegeneration and to develop novel therapeutic strategies for the treatment of age-related brain pathology.Цель исследования — разработка батареи тестов, направленных на изучение социальных и когнитивных нарушений при физиологической нейродегенерации, для поведенческого фенотипирования стареющих экспериментальных животных. Исследовали аутбредных мышей-самцов линии CD1, из которых были сформированы две группы: 1-я основная (физиологическое старение) — животные в возрасте 12 мес, 2-я контрольная — мыши в возрасте 2 мес. Для оценки неврологического статуса животных использовали такие поведенческие тесты, как социальный пятипопыточный тест, «Приподнятый крестообразный лабиринт», тест «Открытое поле», тест «Черно-белая камера», тест «Fear conditioning». Анализ результатов социального пятипопыточного теста показал снижение заинтересованности особью противоположного пола у стареющих животных по сравнению с контрольной группой. У основной группы в тестах «Приподнятый крестообразный лабиринт» и «Черно-белая камера» выявлено повышение уровня тревожности по сравнению с контрольной группой, в тесте «Открытое поле» — низкая двигательная активность и повышенная тревожность. Результаты теста «Fear conditioning» показали, что физиологическая нейродегенерация сопровождается нарушением ассоциативного обучения и запоминания у мышей-самцов, в частности, существенно подавляется процесс консолидации памяти страха. Анализ поведенческих факторов, социального взаимодействия и уровня тревожности у крыс основной группы подтвердил модель возрастной нейродегенерации у стареющих животных. Определены наиболее информативные поведенческие тесты, а именно: «Открытое поле», «Черно-белая камера», «Fear conditioning», позволяющие выявить типичные для стареющих животных векторы поведения — нарушение социальных контактов и взаимодействия, ограничение интересов, повышение уровня тревожности. Это дает возможность получить не только новые фундаментальные знания поведенческих черт модели возрастной нейродегенерации, но и разработать новые терапевтические стратегии для лечения возрастзависимых заболеваний головного мозга.

The review contains current data on molecular mechanisms which control NAD+ homeostasis in brain cells. It also deals with the role of NAD+-converting enzymes in regulation of functional activity, viability and intercellular communication of neuronal and glial cells. Special attention is paid to involvement of CD38 into regulation of NAD+ levels in brain cells in normal and pathological conditions.

Physicocemical and antigenic properties of peripheral blood lymphocytes and shed membrane microparticles were studied in patients with CHD and angina of effort and in those with hypertensive disease. The frequency of lymphocyte blebbing in CHD and angina patients was significantly higher than in those with HD (70.56, 52, 25.7% respectively). Incubation with rotenone and zymosan resulted in an increase of lymphocyte blebbing to 77.34 and 86.5% vs the initial level of 70.56% (p0.05). Patients of both groups had an increased number of membrane microparticles in peripheral blood (59.6 and 78.2 U/4 cm2 respectively). It is concluded that modulation of Imphocyte blebbing and microparticle shedding may be a promising target of cardiovascular prophylaxis.

The role of P2X7 receptors in modulation of the functional activity of macrophages in mice with model peritonitis has been studied. It is established that the functional activity of murine macrophages under such conditions is increased, which is accompanied by the growth of P2X7(+) macrophages and a bidirectional change of the their functional activity under the action of P2X7 modulators. The role of P2X7-associated mechanisms in regulation of the macrophage activity during inflammation is discussed.