Abstract

Background

Atherosclerosis (AS) poses a pressing challenge in contemporary medicine. Glycolysis is a crucial bioenergetic metabolic pathway that provides the primary energy source for endothelial cells. Resveratrol (Res) is a natural compound that has been shown to possess AS. However, the underlying mechanisms of its anti-atherosclerotic effects are not yet fully understood.

Methods

We established a balloon injury model of the common carotid artery in Sprague-Dawley (SD) rats and an ox-LDL endothelial cell injury model for in vivo and in vitro experiments, respectively.

Results

Our study showed that 14 days after balloon-induced injury to the carotid intima of SD rats in vitro, the levels of glycolysis-related proteins fructose-2,6-bisphosphatase 3 (PFKFB3), glucose transporter 1 (GLUT1) and hexokinase 2 (HK2) were increased. Meanwhile, Res treatment improved intimal hyperplasia and reduced the levels of expression of these glycolysis-related proteins, and with higher concentrations of Res leading to more pronounced improvements. In vivo, in ox-LDL HUVECs, Res reduced glucose uptake and lactate production, inhibited apoptosis, and decreased the expression of PFKFB3, GLUT1, HK2, and p-AKT. After the addition of a phosphatidylinositol 3-kinase (PI3K) inhibitor, the we established a balloon injury model of the common carotid artery in SD rats and an ox-LDL endothelial cell injury model for in vivo and in vitro experiments, respectively, and expression levels of p-AKT were observed to increase.

Conclusion

According to these findings, Resveratrol can reduce AS by influencing glycolysis and inhibiting apoptosis through the PI3K-AKT signalling pathway.

Details

Title
The relevance of resveratrol in ameliorating carotid atherosclerosis through glycolysis
Author
Pan, Henan; Wu, Zongkai; Gao, Yaran; Yao, Wentao; Ge, Feng; Wang, Hebo
Pages
1-14
Section
Research
Publication year
2025
Publication date
2025
Publisher
BioMed Central
e-ISSN
14712261
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
3201517867
Copyright
© 2025. This work is licensed under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.