Abstract
The aim of this study was to compare the protective effects of three dietary flavonoids (apigenin-7-O-glucoside (A7G), isorhamnetin-3-O-rutinoside (I3R), and cyanidin-3-O-glucoside (C3G)) on advanced glycation end products (AGEs)-induced inflammation and vascular endothelial dysfunction. Furthermore, the potential mechanisms of varied effects of those three dietary flavonoids were analyzed by molecular docking analysis. Results showed that C3G (40 μM) achieved the best inhibition on inflammatory cytokines (TNF-α, IL-1β, and IL-6) in AGEs-induced RAW264.7 cells, followed by I3R, and A7G was the weakest. The molecular docking results also showed that C3G exhibited the closest binding with the receptor for AGE. However, I3R (40 μM) demonstrated the best effect in improving endothelial dysfunction in AGEs-induced EA.hy926 cells, followed by C3G, and A7G was the weakest, as evidenced by the molecular docking results of flavonoids with profilin-1. This work may provide knowledge and helpful suggestions regarding the benefits of dietary flavonoids in diabetic vascular complications.
Highlights
Type 2 diabetes mellitus (T2DM) is a serious and common global disease that affects more than 360 million people worldwide [1]
The overproduction of reactive oxygen species (ROS) caused by advanced glycation end products (AGEs) is considered a trigger for inflammation and vascular endothelial (VE)-cadherin endocytosis associated with the maintenance of the cytoskeleton [4,7]
We found that apigenin-7-O-glucoside (A7G), isorhamnetin3-O-rutinoside (I3R), and cyanidin-3-O-glucoside (C3G) were the three most effective flavonoids for inhibiting the activities of α-glucosidase and dipeptidyl peptidase-IV and improving insulin resistance among more than 20 dietary flavonoids that may be beneficial for diabetic patients in controlling blood glucose [12,13]
Summary
Type 2 diabetes mellitus (T2DM) is a serious and common global disease that affects more than 360 million people worldwide [1]. Vascular complications are considered one of the leading causes of death from diabetes. Studies have reported that AGEs are believed to be key factors that promote vascular damage and inflammation through receptor-independent and receptor-dependent mechanisms, leading to a series of vascular complications [5,6]. AGEs can induce endothelial cell damage through profilin-1 (PFN1), causing the reorganization and redistribution of endothelial cytoskeleton actin and leading to endothelial cell dysfunction [6]. The overproduction of reactive oxygen species (ROS) caused by AGEs is considered a trigger for inflammation and vascular endothelial (VE)-cadherin endocytosis associated with the maintenance of the cytoskeleton [4,7]. Finding nontoxic and high-efficiency dietary bioactive compounds to improve AGEs-induced inflammation and endothelial dysfunction may be an effective strategy for preventing or alleviating chronic diseases caused by the vascular complications of diabetes
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
