Caffeic Acid Inhibits the Formation of Advanced Glycation End Products (AGEs) and Mitigates the AGEs‐Induced Oxidative Stress and Inflammation Reaction in Human Umbilical Vein Endothelial Cells (HUVECs)

Abstract

The advanced glycation end products (AGEs) are the compounds produced by non‐enzymatic glycation reaction of proteins and sugars, which can induce the generation of free radicals and the expression of inflammatory factors, thereby playing an important role in vascular dysfunction in diabetes. To investigate the effects of caffeic acid (CA) on glycation formed by glucose and protein, various spectroscopic techniques and molecular docking methods were carried out. Furthermore, the protective effects of CA on human umbilical vein endothelial cells (HUVECs) damaged by AGEs were detected. The results indicated that CA inhibited AGEs formation in vitro, decreased the expression of IL‐1β, IL‐18, ICAM‐1, VCAM‐1, NLRP3, Caspase‐1 and CRP (C‐reactive protein) and reduced the ROS in HUVECs exposed to AGEs. Our findings suggested that the supplementation with dietary CA could prevent and delay the AGEs‐induced vascular dysfunction in diabetes.

Bioactive Compounds from Ephedra fragilis: Extraction Optimization, Chemical Characterization, Antioxidant and AntiGlycation Activities

“…It was clearly showed that the native BSA exhibits a characteristic peak at nm, which is mostly due to the aromatic amino acids, including tyrosine, tryptophan, and phenylalanine [ 47 ].…”

Protective effects of phenolic acid extract from ginseng on vascular endothelial cell injury induced by palmitate via activation of PI3K/Akt/eNOS pathway

“…Vanillic acid has the potential to attenuate hypertension, dyslipidemia, and hepatic and renal damage in NO‐deficient rats (Kumar, Prahalathan, Saravanakumar, & Raja, 2014) and alleviates PA‐induced oxidative stress in human umbilical vein endothelial cells (Ma et al., 2019). Caffeic acid has been reported to modulate endothelial NO production and protect against oxidative stress‐associated endothelial cell injury (Cao et al., 2019; Migliori et al., 2015). As a natural source of these phenolic acids, ginseng‐derived PG2 might have the potential to protect endothelial function.…”

Role of the NLRP3 Inflammasome in Preeclampsia

“…AGE-RAGE interactions may increase and perpetuate the inflammatory condition, leading to obesity, diabetes mellitus, and cardiovascular and kidney diseases. Both in vivo and in vitro experiments have demonstrated that AGEs stimulate NLRP3 inflammasome activation and IL-1β secretion in human umbilical vein endothelial cells, kidney, and pancreatic islets (117,156,157). Ablation of the NLRP3 inflammasome improved AGE-induced abnormal insulin sensitivity, pancreatic islet damage, and inflammatory responses (158).…”