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 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 The role of oxidative stress and effect of alpha-lipoic acid in reexpansion pulmonary edema – an experimental study

2010 ◽  
Vol 6 ◽  
pp. 848-853 ◽  
Author(s):  
Seyfettin Gumus ◽  
Orhan Yucel ◽  
Mehmet Gamsizkan ◽  
Ayse Eken ◽  
Omer Deniz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Experimental Study ◽  
Pulmonary Edema ◽  
Lipoic Acid ◽  
Alpha Lipoic Acid ◽  
Reexpansion Pulmonary Edema

scholarly journals The Protective Role of Prenatal Alpha Lipoic Acid Supplementation against Pancreatic Oxidative Damage in Offspring of Valproic Acid-Treated Rats: Histological and Molecular Study

Biology ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 239
Author(s):  
Fatma M. Ghoneim ◽  
Hani Alrefai ◽  
Ayman Z. Elsamanoudy ◽  
Salwa M. Abo El-khair ◽  
Hanaa A. Khalaf
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Lipoic Acid ◽  
Caspase 3 ◽  
Protective Role ◽  
Alpha Lipoic Acid ◽  
Group Iii ◽  
Rat Offspring ◽  
Group I

Background: Sodium valproate (VPA) is an antiepileptic drug (AED) licensed for epilepsy and used during pregnancy in various indications. Alpha-lipoic acid (ALA) is a natural compound inducing endogenous antioxidant production. Our study aimed to investigate the effect of prenatal administration of VPA on the pancreas of rat offspring and assess the potential protective role of ALA co-administration during pregnancy. Methods: Twenty-eight pregnant female albino rats were divided into four groups: group I (negative control), group II (positive control, ALA treated), group III (VPA-treated), and group IV (VPA-ALA-treated). The pancreases of the rat offspring were removed at the fourth week postpartum and prepared for histological, immune-histochemical, morphometric, molecular, and oxidative stress marker studies. Results: In group III, there were pyknotic nuclei, vacuolated cytoplasm with ballooning of acinar, α, and β cells of the pancreas. Ultrastructural degeneration of cytoplasmic organelles was detected. Additionally, there was a significant increase in oxidative stress, a decrease in insulin-positive cell percentage, and an increase in glucagon positive cells in comparison to control groups. Moreover, VPA increased the gene expression of an apoptotic marker, caspase-3, with a decrease in anti-apoptotic Bcl2 and nuclear factor erythroid 2-related factor 2 (Nrf2) transcriptional factor. Conversely, ALA improved oxidative stress and apoptosis in group VI, and a consequent improvement of the histological and ultrastructure picture was detected. Conclusion: ALA co-administration with VPA significantly improved the oxidative stress condition, histological and morphometric picture of the pancreas, and restored normal expression of related genes, including Nrf2, caspase-3, and Bcl-2. Administration of α-lipoic acid has a protective effect against VPA-induced pancreatic oxidative damage via its cytoprotective antioxidant effect.

scholarly journals Alpha lipoic acid attenuates oxidative stress-induced damage macromolecules in the brain of rats with sepsis-associated encephalopathy

Critical Care ◽  
2014 ◽  
Vol 18 (S2) ◽  
Author(s):  
LG Danielski ◽  
M Michels ◽  
D Florentino ◽  
A Viera ◽  
A Lauriano ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipoic Acid ◽  
Alpha Lipoic Acid ◽  
The Brain

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.

Role of Catalase and Superoxide Dismutase Activities on Oxidative Stress in the Brain of a Phenylketonuria Animal Model and the Effect of Lipoic Acid

2012 ◽  
Vol 33 (2) ◽  
pp. 253-260 ◽  
Author(s):  
Tarsila Barros Moraes ◽  
Carlos Eduardo Diaz Jacques ◽  
Andrea Pereira Rosa ◽  
Giovana Reche Dalazen ◽  
Melaine Terra ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Animal Model ◽  
Superoxide Dismutase ◽  
Lipoic Acid ◽  
The Brain

Acute Exercise and Thioredoxin-1 in Rat Brain, and Alpha-Lipoic Acid and Thioredoxin-Interacting Protein Response, in Diabetes

2010 ◽  
Vol 20 (3) ◽  
pp. 206-215 ◽  
Author(s):  
Zekine Lappalainen ◽  
Jani Lappalainen ◽  
David E. Laaksonen ◽  
Niku K.J Oksala ◽  
Savita Khanna ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipoic Acid ◽  
Acute Exercise ◽  
Exhaustive Exercise ◽  
Favorable Effect ◽  
Alpha Lipoic Acid ◽  
Interacting Protein ◽  
Protein Response ◽  
Response To Exercise ◽  
The Brain

Thioredoxin (TRX) is a protein disulfide reductase that plays an important role in many thiol-dependent cellular reductive processes, antioxidant protection, and signal transduction. Moreover, TRX reduces and maintains the function of many proteins during oxidative stress, which is increased in diabetes. The authors recently reported that diabetes impairs brain redox status and TRX response to exercise training. As a continuation of their studies, they hypothesized that alpha-lipoic acid, a natural thiol antioxidant, has a favorable effect on the brain TRX and glutathione (GSH) system in diabetes. Streptozotocin-induced diabetes was used as a chronic model and exhaustive exercise as an acute model for disrupted redox balance. Half the diabetic and nondiabetic animals were subjected to a bout of exhaustive exercise after 8 wk with or without lipoic acid and analyzed for key thiol antioxidants. Lipoic acid neither altered diabetes-induced oxidative stress as assessed by the increased ratio of oxidized to total GSH nor had any impact on the antioxidant protein response to exercise. However, lipoic acid increased mRNA of TRX-interacting protein, an inhibitor of TRX-1, and glutaredoxin-1 in diabetes. Exercise increased TRX-1 mRNA in both diabetic and nondiabetic animals but had no effect on TRX-1 protein. Cytosolic superoxide dismutase mRNA was only increased in diabetes, whereas exercise increased the protein levels in nondiabetic animals. The findings suggest that exhaustive exercise induces mRNA of TRX-1 in the brain and that lipoic acid cannot prevent diabetes-induced disturbances in GSH homeostasis. Because lipoic acid increased TRX-interacting protein transcription in diabetes, high doses may impair TRX-1 homeostasis.

Sign in / Sign up

Export Citation Format

Share Document