scholarly journals Violation in the axis of the "microbiota of the digestive tract-brain" under conditions of ischemia-reperfusion of the brain (literature review)

2021 ◽  
Vol 11 (5) ◽  
pp. 325-332
Author(s):  
O. Tkachuk ◽  
S. Tkachuk ◽  
M. Povar ◽  
O. Denysenko ◽  
V. Shtefaniuk
Keyword(s):  
Literature Review ◽  
Intestinal Microbiota ◽  
Brain Injuries ◽  
Ischemia Reperfusion ◽  
T Cell Homeostasis ◽  
Ischemic Brain ◽  
Intestinal Lymphocytes ◽  
And Migration ◽  
The Brain

The aim of the study is to analyze current views concerning interrelations between the state of intestinal microbiota and the course of ischemic-reperfusion brain injury.   Conclusion. Literary data are indicative of disputable scientific opinions existing nowadays concerning the role of dysbacteriosis (neuroprotective or neurodegenerative) in the course of ischemic brain injuries. Meanwhile, the studies are in common concerning the evidenced role of the intestinal microbiota in disturbances of T-cell homeostasis, ratio changes of their Treg-Th17 subpopulations, and migration of intestinal lymphocytes to the ischemic brain.  

scholarly journals CAUSATIVE-INVESTIGATORY RELATIONSHIPS BETWEEN BOWELS MICROBIOTA AND CLINICAL COURSE OF ISCHEMIA-REPERFUSION DAMAGE OF THE BRAIN

2021 ◽  
Vol 19 (4) ◽  
Author(s):  
S.S. Tkachuk ◽  
M.A. Povar ◽  
V.I. Shtefaniuk ◽  
O.V. Tkachuk
Keyword(s):  
T Cells ◽  
Cerebral Ischemia ◽  
Clinical Course ◽  
Ischemia Reperfusion ◽  
Current Data ◽  
Experimental Investigations ◽  
Ischemic Brain ◽  
Ratio Change ◽  
And Migration ◽  
The Brain

The purpose – to carry out the analysis of the current data concerning relationships inthe “bowels microbiota-brain” system at ischemia-reperfusion damages of the brain.Conclusions.1. The analysis of the literature data testify to the views discrepancy, existing today, on therole of the bowels dysbacteriosis (neuroprotective or neurodegenerative) in the clinicalcourse of ischemic damages of the brain.2. Numerous experimental investigations substantiated the bowels microbiota role:homeostasis derangements of T-cells, which have the determined role in the secondaryneuroinflammation following cerebral ischemia; in the ratio change of their subpopulationsTreg-Th17 and migration of the bowels lymphocytes into the ischemic brain.

scholarly journals Repression of the Glucocorticoid Receptor Aggravates Acute Ischemic Brain Injuries in Adult Mice

2018 ◽  
Vol 19 (8) ◽  
pp. 2428 ◽  
Author(s):  
Yong Li ◽  
Lei Huang ◽  
Qingyi Ma ◽  
Katherine Concepcion ◽  
Minwoo Song ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Brain Injuries ◽  
Expression Profiles ◽  
Control Group ◽  
Ischemic Brain ◽  
Expression Levels ◽  
Adult Mice ◽  
Neurobehavioral Deficits ◽  
The Brain

Strokes are one of the leading causes of mortality and chronic morbidity in the world, yet with only limited successful interventions available at present. Our previous studies revealed the potential role of the glucocorticoid receptor (GR) in the pathogenesis of neonatal hypoxic-ischemic encephalopathy (HIE). In the present study, we investigate the effect of GR knockdown on acute ischemic brain injuries in a model of focal cerebral ischemia induced by middle cerebral artery occlusion (MCAO) in adult male CD1 mice. GR siRNAs and the negative control were administered via intracerebroventricular (i.c.v.) injection 48 h prior to MCAO. The cerebral infarction volume and neurobehavioral deficits were determined 48 h after MCAO. RT-qPCR was employed to assess the inflammation-related gene expression profiles in the brain before and after MCAO. Western Blotting was used to evaluate the expression levels of GR, the mineralocorticoid receptor (MR) and the brain-derived neurotrophic factor/tropomyosin receptor kinase B (BDNF/TrkB) signaling. The siRNAs treatment decreased GR, but not MR, protein expression, and significantly enhanced expression levels of pro-inflammatory cytokines (IL-6, IL-1β, and TNF-α) in the brain. Of interest, GR knockdown suppressed BDNF/TrkB signaling in adult mice brains. Importantly, GR siRNA pretreatment significantly increased the infarction size and exacerbated the neurobehavioral deficits induced by MCAO in comparison to the control group. Thus, the present study demonstrates the important role of GR in the regulation of the inflammatory responses and neurotrophic BDNF/TrkB signaling pathway in acute ischemic brain injuries in adult mice, revealing a new insight into the pathogenesis and therapeutic potential in acute ischemic strokes.

scholarly journals New cerebrovascular agent with hypotensive activity

2019 ◽  
Vol 5 (2) ◽  
pp. 71-77
Author(s):  
Galina A. Kim ◽  
Tamara S. Gan’shina ◽  
Elena V. Kurza ◽  
Ilya N. Kurdyumov ◽  
Denis V. Maslennikov ◽  
...  
Keyword(s):  
Blood Flow ◽  
Antihypertensive Agent ◽  
Brain Injuries ◽  
Cerebrovascular Disorders ◽  
Male Rats ◽  
Hypotensive Activity ◽  
Duration Of Action ◽  
Ischemic Brain ◽  
Cerebrovascular Activity ◽  
The Brain

Introduction: In cerebrovascular disorders, special attention is paid to a hypertensive cerebrovascular crisis, which combines a vascular injury of the brain and hypertension. The paper studies the cerebrovascular properties of the calcium channel blocker of S-Amlodipine nicotinate antihypertensive agent. Materials and methods: Tests were performed on 96 nonlinear male rats, measuring local blood flow in the cerebral cortex in 36 awake animals, using a laser Doppler flowmeter. Cerebral circulation was recorded in the animals when modeling ischemic and hemorrhagic brain injuries. Results and discussion: S-Amlodipine nicotinate (0.1 mg/kg i/v) shows a pronounced cerebrovascular activity in the models of ischemic and hemorrhagic injuries of the brain. In terms of the vasodilating effect in ischemic brain injury, the drug is comparable to mexidol, nimodipine, picamilon, but is superior to nimodipine and picamilon in terms of duration of action, and in the model of hemorrhagic stroke, S-Amlodipine nicotinate is superior to nimodipine and is comparable to picamilon and mexidol. The analysis of the mechanism of action of the agent revealed the participation of GABA A-receptors in the implementation of cerebrovascular properties of the agent. Conclusion: Significant cerebrovascular activity of S-Amlodipine nicotinate (0.1 mg/kg i/v) antihypertensive agent was revealed. The presence of GABAergic mechanism on cerebral blood flow in the agent action along with blockade of slow calcium channels ensures its high efficacy in treatment of both ischemic and hemorrhagic brain injuries.

scholarly journals Role of Acupuncture in the Management of Severe Acquired Brain Injuries (sABIs)

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Loredana Cavalli ◽  
Lucia Briscese ◽  
Tiziana Cavalli ◽  
Paolo Andre ◽  
Maria Chiara Carboncini
Keyword(s):  
Brain Injuries ◽  
Neuronal Regeneration ◽  
Asian Countries ◽  
Rehabilitative Treatment ◽  
Beneficial Effects ◽  
Nervous System Activity ◽  
Neurologic Disorders ◽  
Central Nervous System Activity ◽  
The Brain

Acupuncture therapy has been used to treat several disorders in Asian countries and its use is increasing in Western countries as well. Current literature assessed the safety and efficacy of acupuncture in the acute management and rehabilitation of patients with neurologic disorders. In this paper, the role of acupuncture in the treatment of acute severe acquired brain injuries is described, acting on neuroinflammation, intracranial oedema, oxidative stress, and neuronal regeneration. Moreover, beneficial effects of acupuncture on subacute phase and chronic outcomes have been reported in controlling the imbalance of IGF-1 hormone and in decreasing spasticity, pain, and the incidence of neurovegetative crisis. Moreover, acupuncture may have a positive action on the arousal recovery. Further work is needed to understand the effects of specific acupoints on the brain. Allegedly concurrent neurophysiological measurements (e.g., EEG) may help in studying acupuncture-related changes in central nervous system activity and determining its potential as an add-on rehabilitative treatment for patients with consciousness disorders.

scholarly journals Concentrations of the Selected Biomarkers of Endothelial Dysfunction in Response to Antiepileptic Drugs: A Literature Review

2019 ◽  
Vol 25 ◽  
pp. 107602961985942 ◽  
Author(s):  
Beata Sarecka-Hujar ◽  
Izabela Szołtysek-Bołdys ◽  
Ilona Kopyta ◽  
Barbara Dolińska ◽  
Andrzej Sobczak
Keyword(s):  
Risk Factors ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Literature Review ◽  
Antiepileptic Drug ◽  
Asymmetric Dimethylarginine ◽  
The Body ◽  
Biochemical Processes ◽  
The Brain

Epilepsy is a disease arising from morphological and metabolic changes in the brain. Approximately 60% of patients with seizures can be controlled with 1 antiepileptic drug (AED), while in others, polytherapy is required. The AED treatment affects a number of biochemical processes in the body, including increasing the risk of cardiovascular diseases (CVDs). It is indicated that the duration of AED therapy with some AEDs significantly accelerates the process of atherosclerosis. Most of AEDs increase levels of homocysteine (HCys) as well as may affect concentrations of new, nonclassical risk factors for atherosclerosis, that is, asymmetric dimethylarginine (ADMA) and homoarginine (hArg). Because of the role of these parameters in the pathogenesis of CVD, knowledge of HCys, ADMA, and hArg concentrations in patients with epilepsia treated with AED, both pediatric and adult, appears to be of significant importance.

Molecular Mechanisms of Ischemic Cerebral Edema: Role of Electroneutral Ion Transport

Physiology ◽  
2009 ◽  
Vol 24 (4) ◽  
pp. 257-265 ◽  
Author(s):  
Kristopher T. Kahle ◽  
J. Marc Simard ◽  
Kevin J. Staley ◽  
Brian V. Nahed ◽  
Pamela S. Jones ◽  
...  
Keyword(s):  
Cerebral Edema ◽  
Molecular Mechanisms ◽  
Cell Volume Regulation ◽  
Cell Swelling ◽  
Ischemic Brain Injury ◽  
Edema Formation ◽  
Ischemic Brain ◽  
The Brain ◽  
Permeability Alterations

The brain achieves homeostasis of its intracellular and extracellular fluids by precisely regulating the transport of solute and water across its major cellular barriers: endothelia of the blood-brain barrier (BBB), choroid plexus epithelia, and neuroglial cell membranes. Cerebral edema, the pathological accumulation of fluid in the brain’s intracellular and extracellular spaces, is a major cause of morbidity and mortality following stroke and other forms of ischemic brain injury. Until recently, mechanisms of cerebral edema formation have been obscure; consequently, its treatment has been empiric and suboptimal. Here, we provide a paradigm for understanding ischemic cerebral edema, showing that its molecular pathogenesis is a complex yet step-wise process that results largely from impaired astrocytic cell volume regulation and permeability alterations in the cerebral microvasculature, both of which arise from pathological changes in the activities of specific ion channels and transporters. Recent data has implicated the bumetanide-sensitive NKCC1, an electroneutral cotransporter expressed in astrocytes and the BBB, in cerebral edema formation in several different rodent models of stroke. Pharmacological inhibition or genetic deficiency of NKCC1 decreases ischemia-induced cell swelling, BBB breakdown, cerebral edema, and neurotoxicity. Combination pharmacological strategies that include NKCC1 as a target might thus prove beneficial for the treatment of ischemic, and potentially other types of, cerebral edema.

scholarly journals Dynamics of Choline-Containing Phospholipids in Traumatic Brain Injury and Associated Comorbidities

2021 ◽  
Vol 22 (21) ◽  
pp. 11313
Author(s):  
Sana Javaid ◽  
Talha Farooq ◽  
Zohabia Rehman ◽  
Ammara Afzal ◽  
Waseem Ashraf ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Brain Injuries ◽  
Structural Integrity ◽  
Preclinical Studies ◽  
Neuronal Transmission ◽  
Expanding Population ◽  
Motorized Vehicles ◽  
The Brain ◽  
And Oxidative Stress

The incidences of traumatic brain injuries (TBIs) are increasing globally because of expanding population and increased dependencies on motorized vehicles and machines. This has resulted in increased socio-economic burden on the healthcare system, as TBIs are often associated with mental and physical morbidities with lifelong dependencies, and have severely limited therapeutic options. There is an emerging need to identify the molecular mechanisms orchestrating these injuries to life-long neurodegenerative disease and a therapeutic strategy to counter them. This review highlights the dynamics and role of choline-containing phospholipids during TBIs and how they can be used to evaluate the severity of injuries and later targeted to mitigate neuro-degradation, based on clinical and preclinical studies. Choline-based phospholipids are involved in maintaining the structural integrity of the neuronal/glial cell membranes and are simultaneously the essential component of various biochemical pathways, such as cholinergic neuronal transmission in the brain. Choline or its metabolite levels increase during acute and chronic phases of TBI because of excitotoxicity, ischemia and oxidative stress; this can serve as useful biomarker to predict the severity and prognosis of TBIs. Moreover, the effect of choline-replenishing agents as a post-TBI management strategy has been reviewed in clinical and preclinical studies. Overall, this review determines the theranostic potential of choline phospholipids and provides new insights in the management of TBI.

scholarly journals The Many Faces of Post-Ischemic Tau Protein in Brain Neurodegeneration of the Alzheimer’s Disease Type

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2213
Author(s):  
Ryszard Pluta ◽  
Stanisław J. Czuczwar ◽  
Sławomir Januszewski ◽  
Mirosław Jabłoński
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Injury ◽  
Cerebral Ischemia ◽  
Tau Protein ◽  
Ischemia Reperfusion ◽  
Disease Type ◽  
Dependent Manner ◽  
Ischemic Brain ◽  
The Brain

Recent data suggest that post-ischemic brain neurodegeneration in humans and animals is associated with the modified tau protein in a manner typical of Alzheimer’s disease neuropathology. Pathological changes in the tau protein, at the gene and protein level due to cerebral ischemia, can lead to the development of Alzheimer’s disease-type neuropathology and dementia. Some studies have shown increased tau protein staining and gene expression in neurons following ischemia-reperfusion brain injury. Recent studies have found the tau protein to be associated with oxidative stress, apoptosis, autophagy, excitotoxicity, neuroinflammation, blood-brain barrier permeability, mitochondrial dysfunction, and impaired neuronal function. In this review, we discuss the interrelationship of these phenomena with post-ischemic changes in the tau protein in the brain. The tau protein may be at the intersection of many pathological mechanisms due to severe neuropathological changes in the brain following ischemia. The data indicate that an episode of cerebral ischemia activates the damage and death of neurons in the hippocampus in a tau protein-dependent manner, thus determining a novel and important mechanism for the survival and/or death of neuronal cells following ischemia. In this review, we update our understanding of proteomic and genomic changes in the tau protein in post-ischemic brain injury and present the relationship between the modified tau protein and post-ischemic neuropathology and present a positive correlation between the modified tau protein and a post-ischemic neuropathology that has characteristics of Alzheimer’s disease-type neurodegeneration.

scholarly journals Role of Neurosonography in evaluation of brain abnormalities in neonates

2021 ◽  
Vol 9 (1) ◽  
pp. 26-30
Author(s):  
Vishwanath Reddy
Keyword(s):  
Cerebral Edema ◽  
Brain Injuries ◽  
Periventricular Leukomalacia ◽  
Brain Abnormalities ◽  
Germinal Matrix ◽  
Congenital Lesions ◽  
High Incidence ◽  
The Brain

Background: Brain damage in preterm infants may result from a series of eventsrather than one specific insult. Maturational characteristics with a failingadaptation capacity may predispose the brain to harmful events during bothintrauterine and extrauterine life. The study aimed to detect anomalies in the brain of neonates with neurosonography. Methods : the studywas conducted on patients with clinically suspected lesions in the brain, undergoing NSG for evaluation of brain abnormalities in Prathima Institute ofmedical sciences, Karimnagar.Neurosonographic examinations were performed through anteriorfontanelle in both the coronal and sagittal planes.The examination started in the coronal plane along the coronal suture, with a transducer angled towards the frontal region. Then brain was examined invarious coronal planes by sweeping the transducer from anterior to posterior. Results : The most common abnormality found on neurosonogram in 3 – 5 days was germinal- matrix haemorrahge comprising n=13 (31%) followed by PVL n=12 (28.6%), cyst n=5 (11.9%), flaring n=5 (11.9%), cerebral edema n=4 (9.5%), congenital lesions n=2 (4.8%) and infections n=1 (2.4%). Follow up scan was performed around 2nd week of life, n=24 (57.1%) neonates were showing normal neurosonogram findings, remaining 18 (43%) showing abnormal findings, which are PVL n=6 (14.3%), GMH n=9 (21.4%), cyst n=1(2.4%), cerebral edema n=1 (2.4%) and congenital lesions n=1 (2.4%). Conclusion: High incidence of brain injuries was detected in babies born less than 32 weeks of gestation, weighing less than 1500 gm. The commonest clinical presentation was seizures followed by absent suckling and lethargy. The abnormalities found on the neurosonogram in our study were germinal matrix hemorrhage, periventricular leukomalacia, cystic PVL, corpus callosum agenesis, and TORCH infection.The mortality rate was high in grade III and grade IV GMH.10-14 days followup scan detected new cases of cystic PVL which were not diagnosed in the initial scan

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