scholarly journals Вплив гіпертиреозу на процеси навчання та стан гліальних проміжних філаментів головного мозку щурів

2014 ◽  
Vol 5 (1) ◽  
pp. 66-70
Author(s):  
S. V. Kyrychenko ◽  
V. S. Nedzvetsky
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Passive Avoidance ◽  
Conditioned Reflex ◽  
Soluble Fraction ◽  
Behavioral Reactions ◽  
Time Saving ◽  
The Brain ◽  
Polypeptide Band

The influence of hyperthyreosis on oxidative stress, state of glial intermediate filaments and memotry was investigated. Significant increasing of lipid peroxidation products into both hippocampus and cortex and change for the worse of memory was observed. Analysis of the behavioral reactions of rats in the test of passive avoidance conditioned reflex showed that the acquisition of skills of all groups of animals did not differ by time waiting period (latent period). Time saving memory test conditioned reflex of passive avoidance was excellent in the group of rats treated with thyroxine compared with controls. The change of polypeptide GFAP was observed in hippocampus and cortex. Both soluble and filamentous forms of GFAP increased in hippocampus of rat with hyperthyreosis. In filament fractions, increase in the intensity of 49 kDa polypeptide band was found. In the same fraction of insoluble cytoskeleton proteins degraded HFKB polypeptides with molecular weight in the region of 46–41 kDa appeared. Marked increase of degraded polypeptides was found in the soluble fraction of the brain stem. The intensity of the intact polypeptide (49 kDa), as well as in the filament fraction, significantly increased. It is possible that increasing concentrations of soluble subunits glial filaments may be due to dissociation of own filaments during the reorganization of cytoskeleton structures. Given the results of Western blotting for filament fraction, increased content of soluble intact 49 kDa polypeptide is primarily the result of increased expression of HFKB and only partly due to redistribution of existing filament structures. Calculation and analysis of indicators showed high correlation between the increase in content and peroxidation products of HFKB. These results indicate the important role of oxidative stress in the induction of astroglial reactive response under conditions of hyperthyroidism. This data shows the possibility of the glial cell cytoskeleton reconstruction under effect of thyroid hormones. 

scholarly journals Neuroprotective effects of α-lipoic acid on the development of oxidative stress and astrogliosis in the brain of STZ-diabetic rats

2014 ◽  
Vol 5 (2) ◽  
pp. 143-147
Author(s):  
S. Kyrychenko ◽  
I. Prishchepa ◽  
V. Lagoda ◽  
M. Velika ◽  
V. Nedzvetsky
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Lipoic Acid ◽  
Diabetic Rats ◽  
Alpha Lipoic Acid ◽  
Neuroprotective Effects ◽  
Neuronal Markers ◽  
The Brain ◽  
Polypeptide Band

The aim of this study was to examine whether the antioxidant alpha-lipoic acid protects neurons from diabetic-reperfusion injury. The streptozotocin (STZ) rat model was used to study the glial reactivity and prevention of gliosis by alpha-lipoic acid (alpha-LA) administration. The expression of glial fibrillary acidic protein (GFAP) was determined, as well as lipid peroxidation (LPO) and glu-tathione (GSH) levels in some brain tissues. We observed significant increasing of lipid peroxidation products in both hippocampus and cortex. Changesof polypeptide GFAP were observed in hippocampus and cortex. Both soluble and filamentous forms of GFAP featured the increase in hippocampus of rat with hyperthyreosis. In the filamentfractions, increase in the intensity of 49 kDa polypeptide band was found. In the same fraction of insoluble cytoskeleton proteins degraded HFKB polypeptides with molecular weight in the range of 46–41 kDa appeared. Markedincrease of degraded polypeptides was found in the soluble fraction of the brain stem. The intensity of the intact polypeptide – 49 kDa, as well as in the filament fraction, significantly increased. It is possible that increasing concentrations of soluble subunits glial filaments may be due to dissociation of own filaments during the reorganization of cytoskeleton structures. Given the results of Western blotting for filament fraction, increased content of soluble intact 49 kDa polypeptide is primarily the result of increased expression of HFKB and only partly due to redistribution of existing filament structures. Calculation and analysis of indicators showed high correlation between the increase in content and peroxidation products of HFKB.These results indicate the important role of oxidative stress in the induction of astroglial response under conditions of diabet encefalopathia. Administration of alpha-LA reduced the expression both of glial and neuronal markers. In addition, alpha-LA significantly prevented the increase in LPO levels found in diabetic rats. GSH levels increased by the administration of alpha-LA. This study suggests that alpha-LA prevents neural injury by inhibiting oxidative stress and suppressing reactive gliosis. All these changes were clearly counteracted by alpha-lipoic acid. The results of this study demonstrate that alpha-lipoic acid provides for protection to the GFAP, as a whole, from diabet -reperfusion injuries. 

scholarly journals Curcumin Reduce Sodium Fluoride-Induced Oxidative Stress in Rat Brain

2018 ◽  
Vol 15 (1) ◽  
pp. 71-77 ◽  
Author(s):  
Nagapuri Kiran Kumar ◽  
Mesram Nageshwar ◽  
Karnati Pratap Reddy
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Oral Administration ◽  
Rat Brain ◽  
Sodium Fluoride ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
The Brain

This study reports the ameliorative role of curcumin against sodium fluoride (NaF) induced oxidative stress in the brain of rats. The rats were divided into control, NaF (20 mg/kg), NaF+Curcumin (20mg/kg) and Curcumin (20mg/kg) groups respectively and treated at everyday interval for 60 consecutive days. Oxidative stress markers in the brain were measured at 60th day. NaF treatment significantly increased LPO content, but decreased the level of GSH and activities of SOD, GPx, and CAT the brain of rats in comparison to the control rats. Oral administration of curcumin to fluoride exposed rats significantly reversed the content of lipid peroxidation, as well as enhanced the level of GSH and SOD, GPx and CAT activities to normal compared to NaF exposed rats. Thus, curcumin showed the potential to prevent sodium fluoride induced oxidative damage in the brain of rats and curcumin may be useful agents against neurodegeneration in the brain.

scholarly journals Insights in the Role of Lipids, Oxidative Stress and Inflammation in Rheumatoid Arthritis Unveiled by New Trends in Lipidomic Investigations

Antioxidants ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 45
Author(s):  
Helena Beatriz Ferreira ◽  
Tânia Melo ◽  
Artur Paiva ◽  
Maria do Rosário Domingues
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Lipid Profile ◽  
Inflammatory Responses ◽  
Molecular Level ◽  
Lipid Hydroperoxides ◽  
Lipid Species ◽  
Inflammatory Autoimmune Disease

Rheumatoid arthritis (RA) is a highly debilitating chronic inflammatory autoimmune disease most prevalent in women. The true etiology of this disease is complex, multifactorial, and is yet to be completely elucidated. However, oxidative stress and lipid peroxidation are associated with the development and pathogenesis of RA. In this case, oxidative damage biomarkers have been found to be significantly higher in RA patients, associated with the oxidation of biomolecules and the stimulation of inflammatory responses. Lipid peroxidation is one of the major consequences of oxidative stress, with the formation of deleterious lipid hydroperoxides and electrophilic reactive lipid species. Additionally, changes in the lipoprotein profile seem to be common in RA, contributing to cardiovascular diseases and a chronic inflammatory environment. Nevertheless, changes in the lipid profile at a molecular level in RA are still poorly understood. Therefore, the goal of this review was to gather all the information regarding lipid alterations in RA analyzed by mass spectrometry. Studies on the variation of lipid profile in RA using lipidomics showed that fatty acid and phospholipid metabolisms, especially in phosphatidylcholine and phosphatidylethanolamine, are affected in this disease. These promising results could lead to the discovery of new diagnostic lipid biomarkers for early diagnosis of RA and targets for personalized medicine.

scholarly journals C60 Fullerene Prevents Restraint Stress-Induced Oxidative Disorders in Rat Tissues: Possible Involvement of the Nrf2/ARE-Antioxidant Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-17 ◽  
Author(s):  
Olga O. Gonchar ◽  
Andriy V. Maznychenko ◽  
Nataliya V. Bulgakova ◽  
Inna V. Vereshchaka ◽  
Tomasz Tomiak ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Protein Expression ◽  
Restraint Stress ◽  
Stress Condition ◽  
Rat Tissues ◽  
Stress Exposure ◽  
The Brain ◽  
Nrf2 Protein

The effects of C60FAS (50 and 500 μg/kg) supplementation, in a normal physiological state and after restraint stress exposure, on prooxidant/antioxidant balance in rat tissues were explored and compared with the effects of the known exogenous antioxidant N-acetylcysteine. Oxidative stress biomarkers (ROS, O2⋅−, H2O2, and lipid peroxidation) and indices of antioxidant status (MnSOD, catalase, GPx, GST, γ-GCL, GR activities, and GSH level) were measured in the brain and the heart. In addition, protein expression of Nrf2 in the nuclear and cytosol fractions as well as the protein level of antiradical enzyme MnSOD and GSH-related enzymes γ-GCLC, GPx, and GSTP as downstream targets of Nrf2 was evaluated by western blot analysis. Under a stress condition, C60FAS attenuates ROS generation and O2⋅− and H2O2 releases and thus decreases lipid peroxidation as well as increases rat tissue antioxidant capacity. We have shown that C60FAS supplementation has dose-dependent and tissue-specific effects. C60FAS strengthened the antiradical defense through the upregulation of MnSOD in brain cells and maintained MnSOD protein content at the control level in the myocardium. Moreover, C60FAS enhanced the GSH level and the activity/protein expression of GSH-related enzymes. Correlation of these changes with Nrf2 protein content suggests that under stress exposure, along with other mechanisms, the Nrf2/ARE-antioxidant pathway may be involved in regulation of glutathione homeostasis. In our study, in an in vivo model, when C60FAS (50 and 500 μg/kg) was applied alone, no significant changes in Nrf2 protein expression as well as in activity/protein levels of MnSOD and GSH-related enzymes in both tissues types were observed. All these facts allow us to assume that in the in vivo model, C60FAS affects on the brain and heart endogenous antioxidative statuses only during the oxidative stress condition.

Integrative view of serpins in health and disease: the contribution of serpinA3

2020 ◽  
Author(s):  
Andrea Sanchez-Navarro ◽  
Isaac González-Soria ◽  
Rebecca Caldiño-Bohn ◽  
Norma A. Bobadilla
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Cellular Processes ◽  
Hormone Transport ◽  
Integrative View ◽  
Health And Disease ◽  
The Brain ◽  
Regulation Of Blood Pressure ◽  
Common Function

Serpins are a superfamily of proteins characterized by their common function as serine protease inhibitors. So far, 36 serpins from nine clades have been identified. These proteins are expressed in all the organs and are involved in multiple important functions such as the regulation of blood pressure, hormone transport, insulin sensitivity, and the inflammatory response. Diseases such as obesity, diabetes, cardiovascular, and kidney disorders are intensively studied to find effective therapeutic targets. Given serpins' outstanding functionality, the deficiency or overexpression of certain types of serpin have been associated with diverse pathophysiological events. In particular, we will focus on reviewing the studies evaluating the participation of serpins, and particularly SerpinA3, in diverse diseases that occur in relevant organs such as the brain, retinas, corneas, lungs, cardiac vasculature, and kidneys. In this review, we summarize the role of serpins in physiological and pathophysiological processes, as well as recent evidence on the crucial role of SerpinA3 in several pathologies. Finally, we emphasize the importance of SerpinA3 in regulating cellular processes such as angiogenesis, apoptosis, fibrosis, oxidative stress, and the inflammatory response.

Role of Vitamins in Neurodegenerative Diseases: A Review

2021 ◽  
Vol 20 ◽  
Author(s):  
Ravi Ranjan Kumar ◽  
Lovekesh Singh ◽  
Amandeep Thakur ◽  
Shamsher Singh ◽  
Bhupinder Kumar
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Vitamin D ◽  
Vitamin C ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Vitamin D Deficiency ◽  
Neurological Disorders ◽  
The Brain

Background: Vitamins are the micronutrients required for boosting the immune system and managing any future infection. Vitamins are involved in neurogenesis, a defense mechanism working in neurons, metabolic reactions, neuronal survival, and neuronal transmission. Their deficiency leads to abnormal functions in the brain like oxidative stress, mitochondrial dysfunction, accumulation of proteins (synuclein, Aβ plaques), neurodegeneration, and excitotoxicity. Methods: In this review, we have compiled various reports collected from PubMed, Scholar Google, Research gate, and Science direct. The findings were evaluated, compiled, and represented in this manuscript. Conclusion: The deficiency of vitamins in the body causes various neurological disorders like Alzheimer’s disease, Parkinson’s disease, Huntington's disease, and depression. We have discussed the role of vitamins in neurological disorders and the normal human body. Depression is linked to a deficiency of vitamin-C and vitamin B. In the case of Alzheimer’s disease, there is a lack of vitamin-B1, B12, and vitamin-A, which results in Aβ-plaques. Similarly, in Parkinson’s disease, vitamin-D deficiency leads to a decrease in the level of dopamine, and imbalance in vitamin D leads to accumulation of synuclein. In MS, Vitamin-C and Vitamin-D deficiency causes demyelination of neurons. In Huntington's disease, vitamin- C deficiency decreases the antioxidant level, enhances oxidative stress, and disrupts the glucose cycle. Vitamin B5 deficiency in Huntington's disease disrupts the synthesis of acetylcholine and hormones in the brain.

Different Role of Lipid Peroxidation in Oxidative Stress-Induced Lethal Injury in Normal and Tumor Thymocytes

1994 ◽  
Vol 312 (1) ◽  
pp. 88-94 ◽  
Author(s):  
P. Palozza ◽  
G. Agostara ◽  
E. Piccioni ◽  
G.M. Bartoli
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation

scholarly journals Apolipoprotein E Antibodies Affect the Retention of Passive Avoidance Memory in the Chick

1998 ◽  
Vol 6 (3) ◽  
pp. 29-40 ◽  
Author(s):  
Chris Lancashire ◽  
Radmila Mileusnic ◽  
Steven P.R. Rose
Keyword(s):  
Risk Factors ◽  
Apolipoprotein E ◽  
Passive Avoidance ◽  
Residence Time ◽  
Memory Formation ◽  
Avoidance Task ◽  
Brain Distribution ◽  
The Brain ◽  
Avoidance Memory

Isoforms of apolipoprotein E (ApoE) have been implicated as risk factors in Alzheimer’s disease. We have, therefore, examined the possible role of ApoE in memory formation, using a one-trial passive avoidance task in day-old chicks. Birds were trained on the task and then at various times pre or post-training were injected intracerebrally with anti-ApoE. Immunofluorescence staining demonstrated the presence of the antibody bound to the neuropil, close to the injection site and adjacent to the ventricle, with a residence time in the brain of up to 30 min. Chicks that were injected 30 min pre-training or just post-training with 5μg/ hemisphere of the antibody learned the task, but were amnesic when tested at 30 min or at subsequent times up to 24 hr Post-training. When tested at 24 hr, birds injected 5.5 hr post-training showed unimpaired retention. Birds injected with 5μg/hemisphere of anti-ApoA-I (which has a brain distribution similar to that of anti-ApoE) at 30 min pretraining showed no amnesia, indicating the specificity of the effect to the ApoE. Possible mechanisms for this effect are discussed.

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