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.
*Department of Nutrition and Health Care, School of Public Health, Fujian Medical University, Fuzhou, Fujian, China
†Center for Reproductive Medicine, Fujian Maternity and Child Health Hospital, Fuzhou, Fujian, China
‡Department of Occupational and Environmental Health, School of Public Health, Fujian Medical University, Fuzhou, Fujian, China.
Reprints: Wenchang Zhang, MD, School of Public Health, Fujian Medical University, 88 Jiaotong Road, Fuzhou 350004, China (e-mail: email@example.com).
Supported by the Natural Science Foundation of Fujian Province (2006J0345), China.
The authors report no conflicts of interest.
Received November 16, 2011
Accepted December 28, 2011