Aging shows a significant relationship with changed vascular structure and function, and advancing age is a major nonmodifiable risk factor in the occurrence of cardiovascular diseases. The senescence of endothelial cells is one of the hallmarks of vascular aging and can induce vascular dysfunction. This study aimed to investigate the effect of total flavonoids (TFs) on human umbilical vein endothelial cells (HUVEC) senescence and identify the potential mechanisms involved. A HUVEC senescence model was induced by angiotensin II. The senescence markers, including senescence-associated β-galactosidase (SA-β-gal), p53, p21, and stagnate G0/G1, were measured. The effects of TFs on miR-34/ SIRT1 were examined by quantitative polymerase chain reaction analysis and Western blot analysis. TFs decreased the percentage of SA-β-gal-positive cells and resulted in G0/G1 cell cycle arrest, while the percentage of cells in the S phase increased. Furthermore, TFs reduced miR-34a expression and increased the expression of SIRT1. After treatment with TFs and a miR-34a inhibitor, the percentage of SA-β-gal-positive cells and the expression of miR-34a decreased, and the expression of SIRT1 increased. The TFs inhibited HUVEC senescence, and the mechanism was related to the miR-34a/Sirtuin1 pathway.
Keywords: HUVEC; SIRT1; miR-34a; senescence; total flavonoids from the Carya cathayensis Sarg. leaves.
© 2019 Wiley Periodicals, Inc.