Biochemical changes related to aging in the brain of rats and the effect of alpha lipoic acid.

2021 ◽  
Vol 0 (0) ◽  
pp. 0-0
Author(s):  
Mohamed El-adl
Critical Care ◽  
2014 ◽  
Vol 18 (S2) ◽  
Author(s):  
LG Danielski ◽  
M Michels ◽  
D Florentino ◽  
A Viera ◽  
A Lauriano ◽  
...  

2010 ◽  
Vol 20 (3) ◽  
pp. 206-215 ◽  
Author(s):  
Zekine Lappalainen ◽  
Jani Lappalainen ◽  
David E. Laaksonen ◽  
Niku K.J Oksala ◽  
Savita Khanna ◽  
...  

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.


2021 ◽  
Author(s):  
Hristian Staykov ◽  
Maria Lazarova ◽  
Yozljam Hassanova ◽  
Miroslava Stefanova ◽  
Lyubka Tancheva ◽  
...  

Abstract This study evaluates some of the neuromodulatory mechanisms of the memory loss preventive effect of alpha-lipoic acid (ALA) in a scopolamine (Sco)-induced rat model of an Alzheimer’s disease (AD) type dementia. Our results confirmed that Sco administration induces significant memory impairment, worsens exploratory behaviour and habituation; it increases acetylcholinesterase (AChE) activity and induces pathological monoamine content changes in the brain prefrontal cortex and hippocampus. ALA administration prevented to a large extent Sco-induced memory impairment; it also improved exploratory behaviour and preserved habituation; it decreased AChE activity, reversing it to Control group levels and corrected aberrant monoamine levels in the brain prefrontal cortex and hippocampus. According to the data available, this is the first time that ALA-induced changes in AChE and monoamine levels in the brain prefrontal cortex and hippocampus (brain structures related to learning and memory) have been demonstrated in a Sco-induced rat model of AD type dementia.


2014 ◽  
Vol 5 (2) ◽  
pp. 143-147
Author(s):  
S. Kyrychenko ◽  
I. Prishchepa ◽  
V. Lagoda ◽  
M. Velika ◽  
V. Nedzvetsky

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. 


PROTOPLASMA ◽  
2010 ◽  
Vol 242 (1-4) ◽  
pp. 49-53 ◽  
Author(s):  
Renu Bist ◽  
Shrilekha Misra ◽  
Devendra K. Bhatt

2020 ◽  
pp. 72-79
Author(s):  
O. A. Gizinger

The role of phosphatidylserine in providing the cognitive functions of the brain is considered. The Neuroexel complex, which contains phosphatidylserine and alpha-lipoic acid, can reduce cognitive imbalance caused by atherosclerotic changes, improve short-term and long-term memory. The use of a dietary supplement, which includes phosphatidylserine, can improve the adaptive potential of a person.


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