Malfunctions of the conjugated system “Restoring thiols – Nitrogen oxide” with acute cerebrovascular accident and possible correction

2015 ◽  
Vol 17 (4) ◽  
Author(s):  
S. V. Horbachova ◽  
I. F. Bielenichev ◽  
L. I. Kucherenko
Keyword(s):  
Brain Tissue ◽  
Nitrosative Stress ◽  
Free Radical Oxidation ◽  
Thiol Group ◽  
Oxidative And Nitrosative Stress ◽  
Radical Oxidation ◽  
Active Mobilization ◽  
Common Carotid Arteries ◽  
The Brain ◽  
Stress Simulation

<p>Experimental acute ischemic stroke was modeled by bilateral occlusion of the common carotid arteries in rats. Antioxidant system in the brain tissue was evaluated by the activity of key enzymes of thiol and disulfide indicators<br />nitrosative stress. Simulation of acute ischemic accompanied by violation of the thiol-disulfide balance and increased nitrotyrosine levels, indicating that the development of oxidative and nitrosative stress in brain tissue. It is established<br />that the use of thiol-containing antioxidants – Thiotriazoline and Angiolin set the highest possible ratio between the levels of reduced and oxidized thiol groups and glutathione, which indicates that the active mobilization of thioldisulfide<br />system in the neutralization products of free-radical oxidation. Identified effects of the drugs used due to the presence in their structure of the thiol group, which contributes to the normalization of the glutathione system in conditions of oxidative stress.</p>

Adaptogenic correction of free radical brain damage in subchronic exposure to sodium fl uoride

2020 ◽  
pp. 381-386
Author(s):  
A. G. Zhukova ◽  
L. G. Gorokhova ◽  
A. S. Kazitskaya ◽  
T. K. Yadykina ◽  
N. N. Mikhailova ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Free Radical ◽  
Brain Tissue ◽  
Free Radical Oxidation ◽  
Radical Oxidation ◽  
Free Radical Processes ◽  
Subchronic Exposure ◽  
Antioxidant Defense Enzymes ◽  
Radical Processes ◽  
Complex Drug

Introduction. Fluorine compounds in small doses, but with prolonged exposure, cause various disorders in organs at the cellular and molecular levels. Activation of free-radical processes plays an important role in the damaging eff ect of fl uorides. Th erefore, one of the most eff ective ways to limit fl uorine-induced damage is to directly aff ect free-radical processes using herbal preparations with antioxidant properties.The aim of the study is to study the eff ect of a dihydroquercetin-based drug on the activity of free radical processes in brain tissue under subchronic exposure to sodium fl uoride (NaF).Materials and methods. Th e work was performed on white male laboratory rats weighing 200-250 g. Th e rats were divided into 3 groups: 1 — control; 2 — rats with chronic exposure to sodium fl uoride (NaF) for 9 weeks; 3 — rats receiving a NAF solution with simultaneous administration of a complex drug based on dihydroquercetin at a dose of 3 mg/kg in 1% starch gel for 3, 6 and 9 weeks. The activity of free radical oxidation and antioxidant defense enzymes — superoxide dismutase (SOD) and catalase-was determined in the cerebral cortex. Th e level of expression of hypoxia-induced transcription factor HIF — 1A and inducible forms of proteins HSP72 and HSP32 were determined in the cytosolic fraction of brain tissue.Results. In the early stages of subchronic fl uoride exposure (1-3 weeks), the expression of protective proteins HIF-1α, HSP72, HSP32 and catalase was shown in the rat cortex, as a result of which the activity of free-radical processes was maintained at the control level. An increase in the timing of fl uoride intake to 9 weeks led to a decrease in antioxidant protection and signifi cant activation of free radical oxidation in brain tissue. Daily administration of a complex drug with dihydroquercetin for 3, 6 and 9 weeks to rats with subchronic fl uoride exposure led to a decrease in the severity of pro- and antioxidant balance disorders in the cerebral cortex. At the same time, the greatest protective eff ect of dihydroquercetin with fl uoride exposure was manifested by the 9th week of its administration.Conclusions. When subchronic intake of fl uorides in the body, the drug based on dihydroquercetin has a neuroprotective eff ect, which is manifested by an increase in the activity of antioxidant enzymes of fr ee radical oxidation and catalase and the resistance of the cortex to induced fr ee radical oxidation.

scholarly journals Influence of neuropeptides acth(4-7)-pro-gly-pro and acth(6-9)-pro-gly-pro on the intensity of redox reactions under experimental depression

2020 ◽  
Vol 10 (3) ◽  
pp. 29-32
Author(s):  
Marina Samotrueva ◽  
Anna Yasenyavskaya ◽  
Aleksandra Tsibizova ◽  
Jumazia Erizhepova ◽  
Nikolai Myasoedov ◽  
...  
Keyword(s):  
Free Radical ◽  
Social Stress ◽  
Redox Reactions ◽  
Antioxidant Properties ◽  
Free Radical Oxidation ◽  
Male Rats ◽  
Radical Oxidation ◽  
Oxidation Processes ◽  
Initial Content ◽  
The Brain

The experiment is devoted to the study of the antioxidant properties of neuropeptides from melanocortins ACTH(4-7)-Pro-Gly-Pro (Semax) and ACTH(6-9)-ProGly-Pro under conditions of experimental depression. The study was carried out on white outbred male rats. In the process of modeling experimental depression (social stress) inter-male confrontations were observed as a result of which groups of animals with aggressive and submissive behaviors were formed. The free radical oxidation processes were assessed by determining the activity of catalase, the initial content of malondialdehyde (MDA), the rate of spontaneous and ascorbate-dependent lipid peroxidation (LPO) in the hypothalamic and prefrontal regions of the brain by spectrophotometric method. It was found that under the influence of melanocortins, there is a pronounced suppression of the processes of free radical oxidation in the hypothalamic and prefrontal regions of the brain, which arose against the background of a stressful load which is manifested by a decrease in the indicators of the oxidative process.

scholarly journals The Changes of Expression and Methylation of Genes Involved in Oxidative Stress in Course of Chronic Mild Stress and Antidepressant Therapy with Agomelatine

Genes ◽  
2020 ◽  
Vol 11 (6) ◽  
pp. 644
Author(s):  
Paulina Wigner ◽  
Ewelina Synowiec ◽  
Paweł Jóźwiak ◽  
Piotr Czarny ◽  
Michał Bijak ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitrosative Stress ◽  
Mononuclear Cells ◽  
Methylation Status ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Oxidative And Nitrosative Stress ◽  
Peripheral Blood Mononuclear ◽  
Taqman Gene Expression Assay ◽  
The Brain

Preclinical studies conducted so far suggest that oxidative stress processes may be associated with the mechanism of depression development. This study shows the effects of chronic administration of agomelatine on expression and the methylation status of Sod1, Sod2, Gpx1, Gpx4, Cat, Nos1, and Nos2 in the brain stricture and blood in the chronic mild stress (CMS) animal model of depression. The animals were exposed to the CMS procedure and treatment with agomelatine (10 mg/kg/day, IP) for five weeks and then were sacrificed. TaqMan Gene Expression Assay, Western blot, and methylation-sensitive high-resolution melting techniques were used to evaluate mRNA and protein expression of the genes, and the methylation status of their promoters. Gpx1, Gpx4, and Sod2 expression in the PBMCs and Sod1 and Sod2 expression in the brain were reduced in the stressed group after agomelatine administration. CMS caused an increase in the methylation of the third Gpx4 promoter in peripheral blood mononuclear cells and Gpx1 promoter in the cerebral cortex. Additionally, stressed rats treated with agomelatine displayed a significantly lower Gpx4 level in the hypothalamus. The results confirm the hypothesis that the CMS procedure and agomelatine administration change the expression level and methylation status of the promoter region of genes involved in oxidative and nitrosative stress.

scholarly journals MicroRNAs, Multiple Sclerosis and Depression

2021 ◽  
Vol 22 (15) ◽  
pp. 7802
Author(s):  
Hsiuying Wang
Keyword(s):  
Multiple Sclerosis ◽  
Depressive Disorders ◽  
Nitrosative Stress ◽  
Mirna Regulation ◽  
Oxidative And Nitrosative Stress ◽  
Relapsing Remitting ◽  
The Central Nervous System ◽  
Patients Experience ◽  
Brain And Spinal Cord ◽  
The Brain

Multiple sclerosis (MS) is a chronic disease of the central nervous system that affects the brain and spinal cord. There are several disease courses in MS including relapsing–remitting MS (RRMS), primary progressive MS (PPMS), and secondary progressive MS (SPMS). Up to 50% of MS patients experience depressive disorders. Major depression (MD) is a serious comorbidity of MS. Many dysfunctions including neuroinflammation, peripheral inflammation, gut dysbiosis, chronic oxidative and nitrosative stress, and neuroendocrine and mitochondrial abnormalities may contribute to the comorbidity between MS and MD. In addition to these actions, medical treatment and microRNA (miRNA) regulation may also be involved in the mechanisms of the comorbidity between MS and MD. In the study, I review many common miRNA biomarkers for both diseases. These common miRNA biomarkers may help further explore the association between MS and MD.

scholarly journals Effectiveness of Brain Protection With Histidine-Tryptophan-Ketoglutarate Solutions

2020 ◽  
Vol 23 (4) ◽  
pp. E510-E516
Author(s):  
Sonay Oğuz ◽  
Halil F. Aşgün ◽  
Başak Büyük
Keyword(s):  
Brain Tissue ◽  
Apoptotic Cell ◽  
Ischemia Reperfusion ◽  
Brain Perfusion ◽  
Tissue Samples ◽  
Ischemia Group ◽  
Htk Solution ◽  
Cerebrovascular Surgery ◽  
Common Carotid Arteries ◽  
The Brain

Background: Tissue-protective solutions increase resistance of cells to ischemic conditions. Especially in carotid and aortic arch surgeries where the brain perfusion is at risk, these solutions may be beneficial to prevent ischemic brain damage. This study was designed to demonstrate the effectiveness of histidine-tryptophan-ketoglutarate (HTK) solution in increasing resistance of brain tissue to ischemic conditions. Methods: Three separate randomized groups were created, each consisting of eight rabbits. The groups were called the ischemia, HTK and sham groups, respectively. In the ischemia group, temporary brain ischemia was created for 15 minutes by placing clamps on the bilateral subclavian and common carotid arteries. Then the clamps were removed, and the brain was reperfused for 30 minutes. In the HTK group, HTK solution was sent to the brain through the internal carotid artery before the same ischemia-reperfusion protocol was applied. Histopathological analyses using a visual scoring system to assess the degree of ischemic changes and the apoptotic cell index by TUNEL test were performed in all brain tissue samples. Results: Apoptotic cell indices of the HTK (20.6%) and sham (17.8%) groups were lower than the ischemia group (56.8%) (P < .05). Statistically significant differences were detected between all groups in categorical scores (P < .05). Conclusions: It was shown that less ischemic damage occurs in the brain tissue with the use of HTK solution, and it may be a candidate approach to prevent the brain from ischemic insults during cerebrovascular surgery. Further studies are required to demonstrate its exact effectiveness, in terms of dose, duration, and temperature.

Propolis Attenuates Nitrosative Stress in the Brain Tissue of Rats Exposed to Total Head Irradiation

2021 ◽  
Vol 24 (4) ◽  
pp. 281-285
Author(s):  
Seyithan Taysi ◽  
◽  
Nour Alafandi ◽  
Elif Demir ◽  
Kadir Çınar ◽  
...  
Keyword(s):  
Brain Tissue ◽  
Nitrosative Stress ◽  
Total Head ◽  
The Brain

scholarly journals Immunohistochemical Study of Antioxidant Enzymes Regulated by Nrf2 in the Models of Epileptic Seizures (KA and PTZ)

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
María Fernanda Munguía-Martínez ◽  
Concepción Nava-Ruíz ◽  
Amairani Ruíz-Díaz ◽  
Araceli Díaz-Ruíz ◽  
Petra Yescas-Gómez ◽  
...  
Keyword(s):  
Antioxidant Enzymes ◽  
Nitrosative Stress ◽  
Epileptic Seizures ◽  
Experimental Models ◽  
Immunohistochemical Expression ◽  
Oxidative And Nitrosative Stress ◽  
Stress Effects ◽  
Spontaneous Seizures ◽  
The Brain

Epilepsy is a neurological disorder characterized by recurrent spontaneous seizures due to an imbalance between cerebral excitability and inhibition, with a tendency towards uncontrolled excitability. Epilepsy has been associated with oxidative and nitrosative stress due to prolonged neuronal hyperexcitation and loss neurons during seizures. The experimental animal models report level of ATP diminished and increase in lipid peroxidation, catalase, and glutathione altered activity in the brain. We studied the immunohistochemical expression and localization of antioxidant enzymes GPx, SOD, and CAT in the rat brains treated with KA and PTZ. A significant decrease was observed in the number of immunoreactive cells to GPx, without significant changes for SOD and CAT in KA-treated rats, and decrease in the number of immunoreactive cells to SOD, without significant changes for GPx and only CAT in PTZ-treated rats. Evident immunoreactivity of GPx, SOD, and CAT was observed mainly in astrocytes and neurons of the hippocampal brain region in rats exposed at KA; similar results were observed in rats treated with PTZ at the first hours. These results provide evidence supporting the role of activation of the Nrf2 antioxidant system pathway against oxidative stress effects in the experimental models of epileptic seizures.

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