Protective Effect of Lipoic Acid against Methylglyoxal-Induced Oxidative Stress in LLC-PK₁ Cells

Abstract

Methylglyoxal (MG), a reactive dicarbonyl compound, is a metabolic byproduct of glycolysis often found at high levels in blood from diabetic patients. The effect of lipoic acid on MG-induced oxidative stress was investigated using LLC-PK₁ renal tubular epithelial cells, which are susceptible to oxidative stress. MG (500 μM) treatment induced LLC-PK₁ cell death to nearly 50% compared with non-treated control cells, but lipoic acid significantly inhibited the MG-induced cytotoxicity in a concentration-dependent manner. In addition, lipoic acid treatment dose-dependently reduced the intracellular reactive oxygen species level increased by 500 μM MG. The nitric oxide level was also increased by 500 μM MG treatment, but it was significantly inhibited by lipoic acid. Furthermore, lipoic acid treatment at 50 μM inhibited the nuclear translocation of nuclear factor-kappa B induced by MG treatment in LLC-PK₁ cells. These findings indicate that lipoic acid has potential as a therapeutic agent against the development of diabetic complications related to MG-induced oxidative stress in diabetes.