Abstract
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.
Highlights
Senescence of endothelial cells (ECs) impairs vascular functions, leading to aging of tissues and organs [1]
[26], we investigated whether transient induce persistent EC senescence, thereby establishing a cellular model for senescence
We evaluated AKT and endothelial nitric oxide synthase (eNOS) activation in order to assess whether the protective effect of Aralia elata (Miq.) Seem (AS) is associated with the AKT/eNOS pathway
Summary
Senescence of endothelial cells (ECs) impairs vascular functions, leading to aging of tissues and organs [1]. Senescence-associated β-galactosidase (SA-β-gal) activity in ECs is widely used as a biomarker for senescence owing to the simplicity of the assay and its apparent specificity for senescent cells [10]. In ECs, hyperglycemia accelerates aging-like processes via SIRT1 downregulation [12], and signal molecules, such as 50 AMP-activated protein kinase (AMPK) involved in the energy sensing pathways, are associated with EC senescence [13]. The phosphoinositide-3-kinase (PI3K)/AKT signaling pathway is crucial in regulating endothelial function and injury [15].
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