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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)
被引:46
|作者:
Cao, Xiangyu
[1
]
Xia, Ying
[1
]
Zeng, Meng
[2
]
Wang, Weiyu
[1
]
He, Yin
[1
]
Liu, Jianli
[1
]
机构:
[1] Liaoning Univ, Sch Life Sci, 66 Chongshan Middle Rd, Shenyang 110036, Peoples R China
[2] Tianjin Acad Environm Sci, 17 Fukang Rd Nankai Dist, Tianjin 300191, Peoples R China
基金:
中国国家自然科学基金;
关键词:
caffeic acid;
advanced glycation end products;
oxidative stress;
vascular dysfunction;
molecular docking;
HUMAN SERUM-ALBUMIN;
CARDIOVASCULAR-DISEASE;
VASCULAR INFLAMMATION;
FREE-RADICALS;
ATHEROSCLEROSIS;
AMINOGUANIDINE;
ANTIOXIDANT;
MODEL;
NEURODEGENERATION;
RELEVANCE;
D O I:
10.1002/cbdv.201900174
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
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-1 beta, 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.
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页数:9
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