Abstract
Senescent cells are considered to be a state of cell cycle arrest after exceeding the ultimate number of cell division, however they still secreting the senescence associated secretory phenotype (SASP) as proinflammatory factors as a sign of metabolically activity.  a certain type of senescence that can be induced by oxidative stress, DNA damage and inflammation this can be called Stress-Induced Premature Senescence (SIPS). Several studies proved that cellular senescence has a massive impact in vivo in aging and aging-related pathophysiology. The main reasons of this phenomenon, which can lead to vascular disorders in endothelial cells, include chronic inflammation, oxidative stress, and diminished nitric oxide bioavailability. Oxidative stress is often linked to many diseases through cell deterioration. It refers to a status where the bioavailability of oxidative stress is much more than the available amount of antioxidant. oxidative stress (ROS) produced by ageing can activate NF-kB and enhance vascular inflammation. To investigate the impact of oxidative stress on endothelial ageing and the assessment of the inflammatory response this study was performed to test the intercellular adhesion molecule (ICAM-1) and the possible correlation with ROS production over a relatively long period of time. Since oxidative stress and premature senescence are correlated and have a major role in endothelial dysfunction this study was performed to investigate the effects of intermittent exposure of HUVECs to H₂O₂ (50µM) on the induction of senescence over a longer period of fifteen days.