Abstract: To investigate the protective effect of theaflavin (TF) on injury of human umbilical vein endothelial cells (HUVEC) induced by hydrogen peroxide (H₂O₂), HUVECs were divided into control group, injury group (0.2 mmol·L^-1 H₂O₂ treatment) and TF pretreatment groups (2.0, 5.0, 10.0 μmol·L^-1+0.2 mmol·L^-1 H₂O₂ treatment). The TF pretreatment groups were pretreated with TF for 2 h. Then, both the injury group and the TF groups were treated with H₂O₂ for 24 h, while the control group was treated with solvent. Cells activity was detected by the MTT method. The levels of lactic dehydrogenase (LDH), nitric oxide (NO), malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) were measured by corresponding detection kits. Reactive oxygen species (ROS), cells apoptosis and protein expression levels were detected using DCFH-DA dying, flow cytometer and Western blot. The results show that cells activity was dramatically decreased in the injury group, and the levels of LDH, cellular ROS, MDA and cells apoptosis increased, while the level of NO and the activities of antioxidant enzymes were declined. TF pretreatment could increase cells’ viability, decrease the level of LDH, maintain the level of NO, and inhibit the increments of ROS and MDA, as well as cells apoptosis. Further study indicated that TF treatment could activate Nrf2/HO-1 signaling pathway, and the inhibitor of Nrf2 could reduce the protective effects of TF on HUVEC cells. In conclusion, TF could alleviate oxidative stress injury in vascular endothelial cells induced by H₂O₂. The mechanism is at least partly associated with the activation of Nrf2/HO-1 pathway.

Key words: theaflavin, vascular endothelial cell, oxidative stress injury, protection mechanism, atherosclerosis