Effects of alpha lipoic acid on motor function and antioxidant enzyme activity of nerve tissue after sciatic nerve crush injury in rats

Abstract

Conclusion: ALA that was given before crush type peripheral nerve injury provided to decrease damage of the nerve. Specific mechanisms of this effect must be clarified and must be shown that it is whether effective when it is given after injury or not.

Amelioration of Metal-Induced Cellular Stress by α-Lipoic Acid and Dihydrolipoic Acid through Antioxidative Effects in PC12 Cells and Caco-2 Cells

“…In recent years, ALA has been studied extensively as a biological antioxidant, detoxification agent, and antidiabetic medicine [ 1 , 5 ]. Moreover, ALA has been claimed to ameliorate age-associated cardiovascular, cognitive, and neuromuscular deficits; it has also been implicated as a modulator of various inflammatory signaling pathways [ 6 , 7 , 8 , 9 , 10 ].…”

Alpha-lipoic acid: mechanisms of action and beneficial effects in the prevention and treatment of diabetic complications

“…Some in vivo and in vitro experimental trials showed that ALA administration increased the intracellular GSH level by 30-70%. 15 ALA antioxidant properties in vitro can be explained in different ways: 1. The concentration of ALA by conduction cell culture studies is often several folds higher than what has been seen in tissues or plasma after a per oral administration.…”

“…[30][31][32] ALA had a protective effect on mitochondrial damage and neurotoxicity caused by chemotherapeutic agents; has protective activity on nervous system lesions caused by chronic constriction injury of the peripheral nerve; topical administration of ALA in a transaction model of sciatic nerve provided faster healing; ALA that was administered 3d before ischemia resulted in a significant protective effect from moderate ischemia-reperfusion injury of the peripheral nerve. 15 The regulatory functions of ALA may now include altering protein S-nitrosylation and regulating the expression of some proteins affected by S-nitrosylation mechanisms. GSH levels were also analyzed and it is proposed that this new mechanism of ALA may be through the regulation of GSH, as this antioxidant protects mitochondrial complexes from NO-induced damage.…”

“…The administration of ALA was followed by decreased iron uptake and its diminished cytosolic reactive pool in cultured lens epithelial cells that was associated with increased cell resistance to a H 2 O 2 challenge and reduction of the iron-induced OS. 12,15,30 ALA treatment of immortalized mouse myoblast cell line (C2C12) myotubes increased the intracellular Ca 2+ concentration, suggesting that ALA may activate AMPK by stimulating the calmodulin-dependent protein kinase kinase (CaMKK) pathway. 12 Another potential benefit of using ALA in the treatment of DM complications is connected with glycation reactions inhibition.…”

“…Acute treatments with ALA were shown to cause to both reduction of expression of NF-κB and matrix metalloproteinase-9, an enzyme responsible for the degradation of the extracellular matrix. 15,[42][43][44] ALA was also found to enhance expression of the insulin receptor substrate 1 (IRS1) protein in muscle of obese Zucker rats, and it also elicited association of IRS1 with the p85 regulatory subunit of PI3K. In skeletal muscle, ALA is proposed to recruit glucose transporter type 4 (GLUT4) from its storage site in the Golgi to the sarcolemma, so that glucose uptake is stimulated by the local increase in transporter abundance.…”