Protective effects of Schisandrin on high glucose-induced changes of RhoA and eNOS activity in human umbilical vein endothelial cells

2018 ◽  
Vol 214 (9) ◽  
pp. 1324-1329 ◽  
Author(s):  
Rong-Jin Zhang ◽  
Hui-Yao Hao ◽  
Qing-Juan Liu ◽  
Hong-Ye Zuo ◽  
Ying-Na Chang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
High Glucose ◽  
Umbilical Vein ◽  
Protective Effects ◽  
Human Umbilical Vein ◽  
Enos Activity ◽  
Umbilical Vein Endothelial Cells ◽  
Induced Changes

scholarly journals SIRT1-Mediated Protective Effect of Aralia elata (Miq.) Seem against High-Glucose-Induced Senescence in Human Umbilical Vein Endothelial Cells

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2625
Author(s):  
Gi Dae Kim
Keyword(s):  
Cell Cycle ◽  
Endothelial Cells ◽  
High Glucose ◽  
Umbilical Vein ◽  
Control Group ◽  
Protective Effects ◽  
Aging Effects ◽  
Human Umbilical Vein ◽  
Aralia Elata ◽  
Umbilical Vein Endothelial Cells

Aralia elata (Miq.) Seem (AS) is widely been for treating many diseases, enhancing energy, and boosting immunity; however, its protective effects against high-glucose (HG)-triggered endothelial dysfunction and the potential underlying mechanisms have not been investigated. In this study, we determined the effect of AS on senescence in human umbilical vein endothelial cells (HUVECs) and elucidated the mechanisms underlying its anti-aging effects. The senescence model of endothelial cells (ECs) was established by culturing HUVECs in media containing HG (30 mM). We found that the proportion of senescent (senescence-associated β-galactosidase+) cells in the HG group was significantly higher than that in the control group; however, this increase was suppressed by AS treatment. Moreover, cell cycle analysis revealed that AS (20 μg/mL) significantly recovered HG-induced cell cycle arrest in ECs, and Western blot revealed that AS prevented HG-induced decreases in silent information regulator 1 (SIRT1) level and endothelial nitric oxide synthase (eNOS) phosphorylation. These results show that AS delayed HG-induced senescence in ECs by modulation of the SIRT1/5′ AMP-activated protein kinase and AKT/eNOS pathways.

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