Abstract
The world faces the serious problem of aging. In this study, we aimed to investigate the effect of chlorogenic acid (CGA) on vascular senescence. C57/BL6 female mice that were 14 ± 3 months old were infused with either Angiotensin II (AngII) or saline subcutaneously for two weeks. These mice were administered CGA of 20 or 40 mg/kg/day, or saline via oral gavage. AngII infusion developed vascular senescence, which was confirmed by senescence associated-β-galactosidase (SA-β-gal) staining. CGA administration attenuated vascular senescence in a dose-dependent manner, in association with the increase of Sirtuin 1 (Sirt1) and endothelial nitric oxide synthase (eNOS), and with the decrease of p-Akt, PAI-1, p53, and p21. In an in vitro study, with or without pre-treatment of CGA, Human Umbilical Vein Endothelial Cells (HUVECs) were stimulated with H2O2 for an hour, then cultured in the absence or presence of 0.5–5.0 μM CGA for the indicated time. Endothelial cell senescence was induced by H2O2, which was attenuated by CGA treatment. Pre-treatment of CGA increased Nrf2 in HUVECs. After H2O2 treatment, translocation of Nrf2 into the nucleus and the subsequent increase of Heme Oxygenase-1 (HO-1) were observed earlier in CGA-treated cells. Furthermore, the HO-1 inhibitor canceled the beneficial effect of CGA on vascular senescence in mice. In conclusion, CGA exerts a beneficial effect on vascular senescence, which is at least partly dependent on the Nuclear factor erythroid 2-factor 2 (Nrf2)/HO-1 pathway.
Highlights
The lifespan of people is increasing worldwide
Systolic blood pressure (SBP) was notably higher in the Angiotensin II (AngII)/saline group compared with the saline/saline group. (Table 2) The favorable effect of chlorogenic acid (CGA) on vascular senescence was canceled by ZnPP in vivo (Figure 5a)
We found for the first time that CGA attenuated vascular senescence, in association with the increase of Sirtuin 1 (Sirt1) and endothelial nitric oxide synthase (eNOS) and with the decrease of p-Akt, plasminogen activator inhibitor-1 (PAI-1), p53, and p21
Summary
The lifespan of people is increasing worldwide. Since the pace of population ageing around the world is getting faster, the prevalence of age-related diseases is on an upward trend. Aging raises socioeconomic problem for countries around the world. In this sense, our society will face an enormous economic challenge in the decades to come. Among senescence-related conditions, vascular senescence has been identified as an important factor underlying diseases such as hypertension, stroke, and arteriosclerosis [1,2,3]. Aging of the vasculature plays a central role in senescence-related diseases [5,6]. Since many cell types never exhaust their maximum replicative potential during their lifespan and fail to present senescence, premature senescence is likely the most important inducer of cellular senescence in vivo [10]. AngII-affected genes are abundant in vascular senescence pathway. AngII-affected genes are abundant in vascular senescence pathway. [13] many papers have reported vascular senescence induced by AngII [14,15,16]
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