Abstract
Aspirin eugenol ester (AEE) possesses anti-thrombotic, anti-atherosclerotic and anti-oxidative effects. The study aims to clarify the mechanism underlying the anti-atherosclerotic effects of AEE on vascular endothelial dysfunction. Both the high-fat diet (HFD)-induced atherosclerotic rat model and the H2O2-induced human umbilical vein endothelial cells (HUVECs) model were used to investigate the effects of AEE on vascular endothelial dysfunction. UPLC/QTOF-MS coupled with a multivariate data analysis method were used to profile the variations in the metabolites of HUVECs in response to different treatments. Pretreatment of HUVECs with AEE significantly ameliorated H2O2-induced apoptosis, the overexpression of E-selectin and VCAM-1, and the adhesion of THP-1 cells. Putative endogenous biomarkers associated with the inhibition of endothelial dysfunction were identified in HUVECs pretreated with AEE in the absence or presence of H2O2, and these biomarkers were involved in important metabolic pathways, including amino acid metabolism, carbohydrate metabolism, and glutathione metabolism. Moreover, in vivo, AEE also significantly reduced vascular endothelial dysfunction and decreased the overexpression of VCAM-1 and E-selectin. Based on our findings, the mechanism underlying the anti-atherosclerotic effects of AEE might be related to a reduction in vascular endothelial dysfunction mediated by ameliorating alterations in metabolism, inhibiting oxidative stress, and decreasing the expression of adhesion molecules.
Highlights
The endothelium has been regarded as a pivotal regulator of vascular homeostasis [1,2].Dysfunctional, activated endothelium induced by various stimuli may increase leukocyte adhesion and the production of cytokines and growth factors, which would promote the development of atherosclerosis, a thrombus and other cardiovascular diseases [3,4,5,6,7,8]
Putative endogenous biomarkers associated with the inhibition of endothelial dysfunction were identified in human umbilical vein endothelial cells (HUVECs) pretreated with Aspirin eugenol ester (AEE) in the absence or presence of H2 O2, and these biomarkers were involved in important metabolic pathways, including amino acid metabolism, carbohydrate metabolism, and glutathione metabolism
The mechanism underlying the anti-atherosclerotic effects of AEE might be related to a reduction in vascular endothelial dysfunction mediated by ameliorating alterations in metabolism, inhibiting oxidative stress, and decreasing the expression of adhesion molecules
Summary
The endothelium has been regarded as a pivotal regulator of vascular homeostasis [1,2]. The mechanism by which AEE regulates cardiovascular diseases remains unknown, many in-vivo studies of AEE have been well documented by our. In‐vitro investigations of AEE with with the application of new technical methods will group [15,17,18]. AEE coupled the application of new technical methods be beneficial for clarifying the the mechanism of action of AEE. Cellular metabolomics has been used to systematically investigate the small‐. Cellular metabolomics is an ideal technical method specific cells [24,25]. Cellular metabolomics is an ideal technical method to probe the effects of to probe the effects of AEE oncell vascular endothelial cellpresent dysfunction. On vascular endothelial the anti-atherosclerotic mechanism of AEE atherosclerotic mechanism of AEE was confirmed in a rat model of HFD‐induced atherosclerosis.
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