Abstract: Objective To investigate the effects of melatonin (MT) on oxidative stress and expression of apoptosis marker protein in human umbilical vein endothelial cells (HUVECs) induced by hydrogen peroxide (H₂O₂). Methods HUVECs were divided into blank group and H₂O₂ (100, 200, 300, 400, 600, 700 mmol/L) groups.CCK8 method was used to select the best concentration for modeling. To clarify the effect of melatonin on oxidative stress injury caused by H₂O₂, HUVECs were divided into control group, H₂O₂ group and melatonin group. Western blot was used to detect the expression of p-p65/p65, SOD2 and cleaved-caspase 3. The activity of super-oxide dismutase (SOD), the concentration of malondialdehyde (MDA) and catalase (CAT) were measred by commercially available kits. Reactive oxygen species (ROS) staining was used to detect ROS content in HUVECs. Results H₂O₂ increased the expression of p-p65/p65 and cleaved-caspase 3(P＜0.001), decreased the expression of SOD2(P＜0.05)its biological activity(P＜0.001) and the concentration of CAT(P＜0.01), elevated the concentration of MDA(P＜0.001) and the level of ROS(P＜0.001)in HUVECs. Compared with H₂O₂ group, MT treatment decreased the expression of p-p65/p65(P＜0.001), SOD2(P＜0.001)and cleaved-caspase 3(P＜0.01), increased the expression of SOD2(P＜0.001)as well as biological activity of SOD(P＜0.001) and the concentration of CAT(P＜0.05) reduced the concentration of MDA(P＜0.001) and the level of ROS(P＜0.001)in HUVECs. Conclusions Melatonin plays a protective role in oxidative stress injury of HUVECs induced by H₂O₂ through up-regulating the expression of SOD2 and down-regulating the expression of p-p65/p65 and cleaved-caspase 3.

Key words: biomedical engineering, melatonin(MT), molecular biology, human umbilical vein endothelial cells (HUVECs), oxidative stress