Protective effects of genistein in homocysteine-induced endothelial cell inflammatory injury.

Hyperhomocysteinemia is a risk factor for cardiovascular disease and the mechanism of homocysteine (HCY)-induced vascular endothelial cell injury has been intensively studied for many years. Recently, a large number of studies have shown inhibitory effects of genistein (GEN), a soy isoflavone, in the process of endothelial cell injury. In the present study, the protective effects of GEN in HCY-induced endothelial cell inflammatory injury were investigated. A model of HCY-induced endothelial cell (ECV-304) inflammatory injury was established in vitro, and the protective effect of GEN in this procession was explored. According to our results, GEN protected HCY-induced endothelial cell from viability decreases, meanwhile prevented the changes of cell morphology and the production of reactive oxygen species (ROS). The expression of NF-kB P-65, IL-6, and ICAM-1 was all down-regulated. During the HCY-induced endothelial cell injury, the endothelial cell apoptosis and proliferation disorder were alleviated. Therefore, we conclude that HCY-induced endothelial cell inflammatory injury could be blocked by GEN. The present findings suggest that GEN protects HCY-induced endothelial cell inflammatory injury may through reducing the release of ROS, inhibiting NF-kB activation, down-regulating the expression of cytokine IL-6 and adhesion molecules ICAM-1, avoiding inflammatory cells and platelet adhesion, accordingly, leading to a balance of endothelial cell proliferation and apoptosis.