The relevance of resveratrol in ameliorating carotid atherosclerosis through glycolysis
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...
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BMC
2025-04-01
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| Series: | BMC Cardiovascular Disorders |
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| Online Access: | https://doi.org/10.1186/s12872-025-04735-3 |
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| author | Henan Pan Zongkai Wu Yaran Gao Wentao Yao Ge Feng Hebo Wang |
| author_facet | Henan Pan Zongkai Wu Yaran Gao Wentao Yao Ge Feng Hebo Wang |
| author_sort | Henan Pan |
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| description | 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. |
| format | Article |
| id | doaj-art-6e636c792f3e43aaa46ac1c2551a2b26 |
| institution | OA Journals |
| issn | 1471-2261 |
| language | English |
| publishDate | 2025-04-01 |
| publisher | BMC |
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| series | BMC Cardiovascular Disorders |
| spelling | doaj-art-6e636c792f3e43aaa46ac1c2551a2b262025-08-20T02:30:19ZengBMCBMC Cardiovascular Disorders1471-22612025-04-0125111410.1186/s12872-025-04735-3The relevance of resveratrol in ameliorating carotid atherosclerosis through glycolysisHenan Pan0Zongkai Wu1Yaran Gao2Wentao Yao3Ge Feng4Hebo Wang5Department of Graduate School, Hebei Medical UniversityDepartment of Neurology, Hebei General Hospital, Affiliated to Hebei Medical UniversityDepartment of Neurology, Hebei General Hospital, Affiliated to Hebei Medical UniversityDepartment of Graduate School, Hebei Medical UniversityDepartment of Graduate School, Hebei Medical UniversityDepartment of Graduate School, Hebei Medical UniversityAbstract 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.https://doi.org/10.1186/s12872-025-04735-3GlycolysisAtherosclerosisVascular diseasesResveratrolPI3K-Akt |
| spellingShingle | Henan Pan Zongkai Wu Yaran Gao Wentao Yao Ge Feng Hebo Wang The relevance of resveratrol in ameliorating carotid atherosclerosis through glycolysis BMC Cardiovascular Disorders Glycolysis Atherosclerosis Vascular diseases Resveratrol PI3K-Akt |
| title | The relevance of resveratrol in ameliorating carotid atherosclerosis through glycolysis |
| title_full | The relevance of resveratrol in ameliorating carotid atherosclerosis through glycolysis |
| title_fullStr | The relevance of resveratrol in ameliorating carotid atherosclerosis through glycolysis |
| title_full_unstemmed | The relevance of resveratrol in ameliorating carotid atherosclerosis through glycolysis |
| title_short | The relevance of resveratrol in ameliorating carotid atherosclerosis through glycolysis |
| title_sort | relevance of resveratrol in ameliorating carotid atherosclerosis through glycolysis |
| topic | Glycolysis Atherosclerosis Vascular diseases Resveratrol PI3K-Akt |
| url | https://doi.org/10.1186/s12872-025-04735-3 |
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