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Ferulic acid inhibits advanced glycation end products (AGEs) formation and mitigates the AGEs-induced inflammatory response in HUVEC cells
- Liu, Jian-li, He, Yong-lin, Wang, Shuai, He, Yin, Wang, Wei-yu, Li, Qi-jiu, Cao, Xiang-yu
- Journal of functional foods 2018 v.48 pp. 19-26
- advanced glycation end products, atherosclerosis, caspase-1, ferulic acid, gene expression, glycation, human umbilical vein endothelial cells, inflammation, intercellular adhesion molecule-1, interleukin-18, interleukin-1beta, messenger RNA, mitogen-activated protein kinase, molecular models, patients, protective effect, signal transduction, spectroscopy, transcription factor NF-kappa B, vascular cell adhesion molecules
- Advanced glycation end products (AGEs) are complex and heterogeneous compounds, which play an important role in diabetic-related vascular complications, especially in atherosclerosis. In this study, the effects of ferulic acid (FA) on glucose-related protein glycation were investigated in vitro by various spectroscopic techniques and molecular docking methods. In order to study the protective effects of FA on AGEs-induced HUVEC cells damage, the mRNA expression of Caspase-1, NLRP3, CRP, ICAM-1, VCAM-1, IL-18 and IL-1β were detected. Moreover, NF-κB and p38 MAPK signaling pathways were analyzed. These results manifested that FA could effectively inhibit the AGEs formation, decrease the AGEs-induced mRNA expression of Caspase-1, NLRP3, CRP, ICAM-1, VCAM-1, IL-18 and IL-1β, and reduce intracellular ROS. FA could mitigate the AGEs-induced inflammatory response in HUVEC cells by suppressing the activation of NF-κB and p38 MAPK signaling pathways. These results suggested that FA might prevent and mitigate the development of atherosclerosis in diabetic patients.