Resveratrol attenuates hydrogen peroxide‑induced apoptosis, reactive oxygen species generation, and PSGL‑1 and VWF activation in human umbilical vein endothelial cells, potentially via MAPK signalling pathways.

Reactive oxygen species (ROS) are implicated in the pathogenesis of thrombosis. Studies have reported that resveratrol exhibits antioxidative activities, however, the effect and underlying mechanisms of resveratrol on venous thrombosis remain largely unknown. To investigate the effect of resveratrol on venous thrombosis and the underlying mechanisms, the present study investigated the effects of resveratrol on cell viability, apoptosis, ROS generation and the expression of thrombosis‑associated markers in human umbilical vein endothelial cells (HUVECs). HUVECs were pretreated with resveratrol for 2 h and incubated with hydrogen peroxide (H2O2) for 24 h prior to the evaluation of cell viability, ROS generation, apoptosis and thrombosis‑associated marker expression by performing MTT assays, 2',7'‑dichlorofluorescin diacetate reagent, flow cytometry, and reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blot analysis, respectively. Subsequently, to validate whether resve-ratrol functions via mitogen‑activated protein kinase (MAPK) pathways, the expression of thrombosis‑associated markers was detected by western blot analysis and RT‑qPCR following treatment of cells with resveratrol and the MAPK pathway activators anisomycin and curcumin. The results demonstrated that cell viability was markedly reduced by H2O2, and resveratrol treatment reversed the reductions in cell viability in a dose‑dependent manner. In addition, the levels of cell apoptosis and ROS generation were significantly increased by H2O2 alone, and resveratrol also reduced these effects in a dose‑dependent manner. Furthermore, the mRNA and protein expression of caspase‑3, P‑selectin glycoprotein ligand‑1 and von Willebrand factor was upregulated by H2O2 treatment in HUVECs. However, resveratrol decreased the protein expression these proteins in a dose‑dependent manner. Resveratrol also significantly inhibited the induction of phosphorylated (p)‑p38, P‑c‑Jun N‑terminal kinase and P‑extracellular signal‑regulated kinase by H2O2, and these effects were attenuated by the MAPK pathway activators anisomycin and curcumin. In conclusion, these results indicate that resveratrol protected HUVECs against oxidative stress and apoptosis. Furthermore, to the best of our knowledge, the present study is the first to demonstrate that resveratrol attenuates the expression of thrombosis‑associated markers induced by H2O2, which may occur through the suppression of the MAPK signalling pathways, indicating a potential novel therapeutic approach to prevent venous thrombosis.