Protective Effect of Theaflavins on Homocysteine-Induced Injury in HUVEC Cells In Vitro

Abstract

A model of homocysteine-induced injury in vascular endothelial cells was established to evaluate the protective role of theaflavins on homocysteine-injured human vascular endothelial cells (HUVECs). The cells were co-incubated with 3 concentrations of theaflavins (5, 10, or 20 mg/L) and 0.5 mM homocysteine for 24 hours. The morphology and viability of the cells were determined, and the DNA damage was detected by a comet assay. Superoxide dismutase, malondialdehyde, glutathione peroxidase, nitric oxide, nitric oxide synthase, and endothelin-1 were measured. The results showed that theaflavins can reduce the changes in and damage of homocysteine-injured HUVECs, increase the viability of homocysteine-injured HUVECs, and alleviate DNA damage induced by homocysteine. These results indicate that theaflavins can inhibit homocysteine-induced injury of HUVECs. Further studies showed that theaflavins may reduce the production of homocysteine-induced reactive oxygen species and partly modulate the secretory dysfunction of vascular endothelial cells caused by homocysteine. This finding indicates that the mechanism by which theaflavins inhibit homocysteine-induced injury may relate to their antioxidant activity and the regulation of the secretion of endothelium-derived factors. These findings suggest that theaflavins may be beneficial in the prevention of atherosclerosis and cardiovascular disease.