Human endothelial senescence induced by IL-1 alpha in vitro

Interleukin 1 (IL-1) is an important proinflammatory cytokine that causes pleiotropic effects. Vascular endothelial cells stimulated by IL-1alpha can lead to the inflammatory response. Reactive oxygen species (ROS) are also generated at the site of inflammation and serve as an important factor against foreign invader. Here we report that long-term stimulation of human vein endothelial cells with IL-1alpha can accelerate their senescence associated with beta-galactosidase activity. The flow cytometric analyses showed that most of the induced cells entered GO-G, phase. DNA damage was more severe in senescent cells by comet assay. The induced cells by IL-1alpha had higher levels of ROS and malonyldialdehyde (MDA), lower activity of antioxidant enzymes and lower capacity of total antioxidant systems than control, which led to cell damage and cell degeneration, that is to say, which contributed to cellular senescence. Our results gave a direct proof to a new hypothesis-"the inflammation hypothesis of aging" on cellular level, and also provided a basis for the study on anti-aging and aging-related diseases.Materials Science, MultidisciplinaryMultidisciplinary SciencesSCI(E)0ARTICLE3218-2221