In the present study, we used TNF-α to stimulate HPAECs to simulate the injury of endothelial cells suffering from chronic heart failure and found that the eNOS activity and NO levels of the cells were decreased, while NAD(P)H oxidase activity and ROS levels were increased, which were also reversed by cell transfection with salusin-β shRNA. The gene discussed is TNF; the disease is congestive heart failure.