RESUMO
Aging is the major risk factor for diseases of the cardiovascular system, such as coronary atherosclerotic heart disease, but little is known about the relationship between atherosclerosis (AS) and agerelated declines in vascular structure and function. Here, we used histological analyses in combination with molecular biology techniques to show that lipid deposition in endothelial cell was accompanied by aging and growth arrest. Endothelial cell senescence is sufficient to cause AS; however, we found that salidroside reduced intracellular lipid deposition, slowed the progression of endothelial cell senescence and inhibited the expression of the senescencerelated molecules and phosphorylated the retinoblastoma (Rb) protein. Further study confirmed that salidroside increased the percent of S phase cells in oxidized lowdensity lipoprotein (oxLDL)treated endothelial cells. Collectively, vascular endothelial cell function declined with age and AS, and our data suggested that salidroside prevented oxLDLtreated endothelial cell senescence by promoting cell cycle progression from G0/G1 phase to S phase via Rb phosphorylation. We demonstrated for the first time the complex interactions between AS and endothelial cell senescence, and we believe that salidroside represents a promising therapy for senescencerelated AS.
