Alpha-lipoic acid ameliorates H 2 O 2 -induced human vein endothelial cells injury via suppression of inflammation and oxidative stress

• Published in: Bioscience, biotechnology, and biochemistry Vol. 84; no. 11; p. 2253
• Main Authors: Wang, Wei, An, Li-Ping, Li, Yun-Feng, An, Ran, Bian, Zhe, Liu, Wei-Zhe, Song, Qiu-Hang, Li, Ai-Ying
• Format: Journal Article
• Language: English
• Published: England 01.11.2020
• Subjects: Apoptosis - drug effects; Cytoprotection - drug effects; Down-Regulation - drug effects; Human Umbilical Vein Endothelial Cells - cytology; Human Umbilical Vein Endothelial Cells - drug effects; Human Umbilical Vein Endothelial Cells - metabolism; Humans; Hydrogen Peroxide - adverse effects; Inflammation - pathology; L-Lactate Dehydrogenase - metabolism; NADPH Oxidase 4 - metabolism; NF-kappa B - metabolism; Oxidative Stress - drug effects; Signal Transduction - drug effects; Thioctic Acid - pharmacology; inflammation; Alpha-lipoic acid; apoptosis; oxidative stress
• ISSN: 1347-6947

The study was aimed to investigate the effect of alpha-lipoic acid (ALA) on human umbilical vein endothelial cells (HUVECs) injury induced by hydrogen peroxide (H O ) and to explore its possible mechanisms. We established the H O -induced HUVECs injury model and the ALA treatment groups in which HUVECs were co-incubated with H O (250 μmol/L) and different final concentrations of ALA (100,200,400 μmol/L) for 48 h. Cell survival rate assay and LDH activity assay were carried out. The levels of related proteins were performed by Western Blot. We observed that H O administration resulted in an increase in the LDH activity and a decrease in cell survival rate. The expression levels of Nox4, Bax, NF-κB p65, Caspase-9, Caspase-3, iNOS, VCAM-1 and ICAM-1 were up-regulated, while the expression level of Bcl-2 was down-regulated. All these factors were significantly improved by ALA treatment. In brief, ALA treatment ameliorates H O -induced HUVECs damage by inhibiting inflammation and oxidative stress.