OBJECTIVE: To investigate the role of lycium bararum polysaccharides (LBP) on angiotensin II (AngII)-induced senescence of human umbilical vein endothelial cells (HUVECs) and expressions of P53 and P16 and explore the mechanism of LBP against aging. METHODS: HUVECs cultured in vitro were stimulated with 1×10(-6) mmol/L AngII to induce cell senescence, which was identified using β-gal staining. Flow cytometry was used for analyzing the cell cycle changes, and the cell viability was assessed using CCK-8 method. Western blotting was employed to detect the expression of P53 and P16 in the exposed cells. RESULTS: Compared with the control cells, the cells positive for β-gal staining was significantly increased in AngII group, and showed cell cycle arrest at G(0)/G(1) phase with decreased S-phase cell percentage and cell viability. The expression levels of P53 and P16 were significantly increased in the cells with AngII exposure (P<0.05). LBP treatment of AngII-exposed cells resulted in decreased β-gal-positive cells with a reduction in G(0)/G(1) phase cells and an increase in S phase cells. LBP treatment also increased the cell viability and significantly decreased the expression levels of P53 and P16 (P<0.05). CONCLUSION: LBP can delay AngII-induced aging of HUVECs possibly by down-regulating the expression of P53 and P15.
OBJECTIVE: To investigate the role of lycium bararum polysaccharides (LBP) on angiotensin II (AngII)-induced senescence of human umbilical vein endothelial cells (HUVECs) and expressions of P53 and P16 and explore the mechanism of LBP against aging. METHODS: HUVECs cultured in vitro were stimulated with 1×10(-6) mmol/L AngII to induce cell senescence, which was identified using β-gal staining. Flow cytometry was used for analyzing the cell cycle changes, and the cell viability was assessed using CCK-8 method. Western blotting was employed to detect the expression of P53 and P16 in the exposed cells. RESULTS: Compared with the control cells, the cells positive for β-gal staining was significantly increased in AngII group, and showed cell cycle arrest at G(0)/G(1) phase with decreased S-phase cell percentage and cell viability. The expression levels of P53 and P16 were significantly increased in the cells with AngII exposure (P<0.05). LBP treatment of AngII-exposed cells resulted in decreased β-gal-positive cells with a reduction in G(0)/G(1) phase cells and an increase in S phase cells. LBP treatment also increased the cell viability and significantly decreased the expression levels of P53 and P16 (P<0.05). CONCLUSION: LBP can delay AngII-induced aging of HUVECs possibly by down-regulating the expression of P53 and P15.