Protective effects of lipoic acid against acrylamide-induced neurotoxicity: involvement of mitochondrial energy metabolism and autophagy

2017 ◽  
Vol 8 (12) ◽  
pp. 4657-4667 ◽  
Author(s):  
Ge Song ◽  
Zhigang Liu ◽  
Luanfeng Wang ◽  
Renjie Shi ◽  
Chuanqi Chu ◽  
...  

Lipoic acid (LA) suppressed acrylamide (ACR)-induced inflammation, redox status disturbance, autophagy, and apoptosis mediated by mitochondria in the SH-SY5Y cells.

2011 ◽  
Vol 89 (6) ◽  
pp. 792-797 ◽  
Author(s):  
Johannes A. Mayr ◽  
Franz A. Zimmermann ◽  
Christine Fauth ◽  
Christa Bergheim ◽  
David Meierhofer ◽  
...  

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1699
Author(s):  
Dmitry S. Semenovich ◽  
Egor Yu. Plotnikov ◽  
Oksana V. Titko ◽  
Elena P. Lukiyenko ◽  
Nina P. Kanunnikova

The glutathione system in the mitochondria of the brain plays an important role in maintaining the redox balance and thiol–disulfide homeostasis, whose violations are the important component of the biochemical shifts in neurodegenerative diseases. Mitochondrial dysfunction is known to be accompanied by the activation of free radical processes, changes in energy metabolism, and is involved in the induction of apoptotic signals. The formation of disulfide bonds is a leading factor in the folding and maintenance of the three-dimensional conformation of many specific proteins that selectively accumulate in brain structures during neurodegenerative pathology. In this study, we estimated brain mitochondria redox status and functioning during induction of oxidative damage in vitro. We have shown that the development of oxidative stress in vitro is accompanied by inhibition of energy metabolism in the brain mitochondria, a shift in the redox potential of the glutathione system to the oxidized side, and activation of S-glutathionylation of proteins. Moreover, we studied the effects of pantothenic acid derivatives—precursors of coenzyme A (CoA), primarily D-panthenol, that exhibit high neuroprotective activity in experimental models of neurodegeneration. Panthenol contributes to the significant restoration of the activity of enzymes of mitochondrial energy metabolism, normalization of the redox potential of the glutathione system, and a decrease in the level of S-glutathionylated proteins in brain mitochondria. The addition of succinate and glutathione precursor N-acetylcysteine enhances the protective effects of the drug.


2016 ◽  
Vol 17 (13) ◽  
pp. 1527-1534 ◽  
Author(s):  
Bárbara J. Henriques ◽  
Tânia G. Lucas ◽  
Cláudio M. Gomes

2020 ◽  
Vol 29 (7) ◽  
pp. 616-622 ◽  
Author(s):  
Attila Oláh ◽  
Majid Alam ◽  
Jérémy Chéret ◽  
Nikolett Gréta Kis ◽  
Zoltán Hegyi ◽  
...  

Function ◽  
2021 ◽  
Author(s):  
Alba Clara Sarti ◽  
Valentina Vultaggio-Poma ◽  
Simonetta Falzoni ◽  
Sonia Missiroli ◽  
Anna Lisa Giuliani ◽  
...  

Abstract Basal expression of the P2X7 receptor (P2X7R) improves mitochondrial metabolism, ATP synthesis and overall fitness of immune and non-immune cells. We investigated P2X7R contribution to energy metabolism and subcellular localization in fibroblasts (mouse embryo fibroblasts and HEK293 human fibroblasts), mouse microglia (primary brain microglia and the N13 microglia cell line), and heart tissue. The P2X7R localizes to mitochondria, and its lack a) decreases basal respiratory rate, ATP-coupled respiration, maximal uncoupled respiration, resting mitochondrial potential, mitochondrial matrix Ca2+ level, b) modifies expression pattern of oxidative phosphorylation (OxPhos) enzymes, and c) severely affects cardiac performance. Hearts from P2rx7-deleted versus WT mice are larger, heart mitochondria smaller, and stroke volume (SV), ejection fraction (EF), fractional shortening (FS) and cardiac output (CO), are significantly decreased. Accordingly, physical fitness of P2X7R-null mice is severely reduced. Thus, the P2X7R is a key modulator of mitochondrial energy metabolism and a determinant of physical fitness.


Dose-Response ◽  
2021 ◽  
Vol 19 (1) ◽  
pp. 155932582110012
Author(s):  
Shaimaa M. Badr-Eldin ◽  
Usama A. Fahmy ◽  
Hibah M. Aldawsari ◽  
Osama A. A. Ahmed ◽  
Nabil A. Alhakamy ◽  
...  

Peptic ulcer disease is an injury of the alimentary tract that leads to a mucosal defect reaching the submucosa. Alpha-lipoic acid (ALA), a natural potent antioxidant, has been known as a gastroprotective drug yet its low bioavailability may restrict its therapeutic efficacy. This study aimed to formulate and optimize ALA using a self-nanoemulsifying drug delivery system (SNEDDS) with a size of nano-range, enhancing its absorption and augmenting its gastric ulcer protection efficacy. Three SNEDDS components were selected as the design factors: the concentrations of the pumpkin oil (X1, 10–30%), the surfactant tween 80 (X2, 20–50%), and the co-surfactant polyethylene glycol 200 (X3, 30–60%). The experimental design for the proposed mixture produced 16 formulations with varying ALA-SNEDDS formulation component percentages. The optimized ALA-SNEDDS formula was investigated for gastric ulcer protective effects by evaluating the ulcer index and by the determination of gastric mucosa oxidative stress parameters. Results revealed that optimized ALA-SNEDDS achieved significant improvement in gastric ulcer index in comparison with raw ALA. Histopathological findings confirmed the protective effect of the formulated optimized ALASNEDDS in comparison with raw ALA. These findings suggest that formulation of ALA in SNEDDS form would be more effective in gastric ulcer protection compared to pure ALA.


Sign in / Sign up

Export Citation Format

Share Document