Evaluation of Ginsenoside Rg1 as a Potential Antioxidant for Preventing or Ameliorating Progression of Atherosclerosis

Purpose: To determine whether Rg1 inhibits H₂O₂-induced injury in human umbilical vein endothelial cells (HUVECs), an injury often regarded as a key early event in the development of atherosclerosis.
Methods: Cell viability of HUVECs treated with Rg1 and/or H₂O₂ was measured using 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide ( MTT) assay. Lactate dehydrogenase (LDH) release, lipid peroxidation, and reserved oxidase were detected using different available kits. The apoptosis pathway involved in the effect of Rg1 was also evaluated.
Results: Exposing HUVECs to 100 μmol/L H₂O₂ significantly decreased cell viability (78.12 ± 1.78 %), nitric oxide production, and nitric oxide synthase, superoxide dismutase, and glutathione activities, but markedly increased malondialdehyde content (from 26.87 ± 3.97 to 45.84 ± 3.50 nmol/mg of protein) and LDH release (from 8.63 to 31.42 %) (p < 0.05). These results were accompanied by a decrease in mitochondrial membrane potential and up-regulation of Bid and caspase-3, -8, and -9 mRNA expressions. However, pretreatment with different Rg1 concentrations (4, 8, and 16 µmol/L) markedly attenuated these changes (p < 0.05).
Conclusion: Rg1 may protect HUVECs against H₂O₂-induced injury via the anti-oxidative and anti-apoptosis mechanisms, which could be applied potentially for the prevention of endothelial cell dysfunctions associated with atherosclerosis.

Keywords
Ginsenoside Rg1; Human umbilical vein endothelium; Oxidative damage; Atherosclerosis