Salidroside slows the progression of EA.hy926 cell senescence by regulating the cell cycle in an atherosclerosis model

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 age-related 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 senescence-related molecules and phosphorylated the retinoblastoma (Rb) protein. Further study confirmed that salidroside increased the percent of S phase cells in oxidized low-density lipoprotein (ox-LDL)-treated endothelial cells. Collectively, vascular endothelial cell function declined with age and AS, and our data suggested that salidroside prevented ox-LDL-treated 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 senescence-related AS.