Advanced age is an independent risk factor for ageing-related complex diseases, such as coronary artery disease, stroke, and hypertension, which are common but life threatening and related to the ageing-associated vas...Advanced age is an independent risk factor for ageing-related complex diseases, such as coronary artery disease, stroke, and hypertension, which are common but life threatening and related to the ageing-associated vascular dysfunction. On the other hand, patients with progeria syndromes suffer from serious atherosclerosis, suggesting that the impaired vascular functions may be critical to organismal ageing, or vice versa. However, it remains largely unknown how vascular cells, particularly endothelial cell, become senescent and how the senescence impairs the vascular functions and contributes to the age-related vascular diseases over time. Here, we review the recent progress on the characteristics of vascular ageing and endothelial cell senescence in vitro and in vivo, evaluate how genetic and envi- ronmental factors as well as autophagy and stem cell influence endothelial cell senescence and how the senescence contributes to the age- related vascular phenotypes, such as atherosclerosis and increased vascular stiffness, and explore the possibility whether we can delay the age-related vascular diseases through the control of vascular ageing.展开更多
Objectives Endothelial senescence has been proposed to be involved in endothelial dysfunction and atherogenesis. This study investigates the effects of ginsenoside Rbl, a major constituent of ginseng,on H<sub>2&...Objectives Endothelial senescence has been proposed to be involved in endothelial dysfunction and atherogenesis. This study investigates the effects of ginsenoside Rbl, a major constituent of ginseng,on H<sub>2</sub>O<sub>2</sub>-induced endothelial senescence.Methods Primary human umbilical vein endothelial cells（HUVECs） senescence was induced by H<sub>2</sub>O<sub>2</sub> as judged by senescence-associated P-galactosidase assay （SA-P-gal）.Fntracellur superoxide dismutase（S0D1） activity and malondialdehyde（MDA） level were determined by commercial kit.S0D1 mRNA and protein expression were analyzed by real time PCR and Western blot.Reactive oxygen species（ROS） were determined by flow cytometry.Results Rb1 was found to reverse endothelial senescence,as witnessed by a significant decrease of senescent cell numbers. Rbl could markedly increase intracellular SOD activity, decrease the MDA level,and suppress the generation of intracellular ROS in H<sub>2</sub>O<sub>2</sub>-treated HUVECs.Consistent with these findings,Rbl can effectively restore SOD1 mRNA and protein expression which decreased in H<sub>2</sub>O<sub>2</sub> treated cells. Conclusions Our report demonstrates thatRbl can exert reversal effects on H<sub>2</sub>O<sub>2</sub>-induced cellular senescence through modulating cellular redox status.展开更多
基金supported by the National Basic Research Program of the Chinese Ministry of Science and Technology to XLT(No.2013CB530700)
文摘Advanced age is an independent risk factor for ageing-related complex diseases, such as coronary artery disease, stroke, and hypertension, which are common but life threatening and related to the ageing-associated vascular dysfunction. On the other hand, patients with progeria syndromes suffer from serious atherosclerosis, suggesting that the impaired vascular functions may be critical to organismal ageing, or vice versa. However, it remains largely unknown how vascular cells, particularly endothelial cell, become senescent and how the senescence impairs the vascular functions and contributes to the age-related vascular diseases over time. Here, we review the recent progress on the characteristics of vascular ageing and endothelial cell senescence in vitro and in vivo, evaluate how genetic and envi- ronmental factors as well as autophagy and stem cell influence endothelial cell senescence and how the senescence contributes to the age- related vascular phenotypes, such as atherosclerosis and increased vascular stiffness, and explore the possibility whether we can delay the age-related vascular diseases through the control of vascular ageing.
文摘Objectives Endothelial senescence has been proposed to be involved in endothelial dysfunction and atherogenesis. This study investigates the effects of ginsenoside Rbl, a major constituent of ginseng,on H<sub>2</sub>O<sub>2</sub>-induced endothelial senescence.Methods Primary human umbilical vein endothelial cells（HUVECs） senescence was induced by H<sub>2</sub>O<sub>2</sub> as judged by senescence-associated P-galactosidase assay （SA-P-gal）.Fntracellur superoxide dismutase（S0D1） activity and malondialdehyde（MDA） level were determined by commercial kit.S0D1 mRNA and protein expression were analyzed by real time PCR and Western blot.Reactive oxygen species（ROS） were determined by flow cytometry.Results Rb1 was found to reverse endothelial senescence,as witnessed by a significant decrease of senescent cell numbers. Rbl could markedly increase intracellular SOD activity, decrease the MDA level,and suppress the generation of intracellular ROS in H<sub>2</sub>O<sub>2</sub>-treated HUVECs.Consistent with these findings,Rbl can effectively restore SOD1 mRNA and protein expression which decreased in H<sub>2</sub>O<sub>2</sub> treated cells. Conclusions Our report demonstrates thatRbl can exert reversal effects on H<sub>2</sub>O<sub>2</sub>-induced cellular senescence through modulating cellular redox status.
