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7-Ethoxyrosmanol alleviates hyperglycemia-induced vascular endothelial dysfunction by regulating FBXL7 expression
Jianqi Ni1, Lan Shen2, Liu Xu1
1Department of Vascular Surgery, The First Hospital of Jiaxing, Affiliated Hospital of Jiaxing University, No. 1882 Zhonghuan South Road, Jiaxing, 314001, Zhejiang, China.
7-Ethoxyrosmanol (7ERM) shows promise for treating hyperglycemia. This compound protects against high glucose-induced endothelial dysfunction by regulating F-box/LRR-repeat protein 7 (FBXL7) expression in human umbilical vein endothelial cells.
Area of Science:
- Biomedical Science
- Pharmacology
- Cell Biology
Background:
- Current hyperglycemia treatments are insufficient, leading to endothelial dysfunction.
- Hyperglycemia-induced endothelial dysfunction is a significant complication requiring novel therapeutic approaches.
Purpose of the Study:
- To investigate the potential of 7-Ethoxyrosmanol (7ERM) as a therapeutic agent for hyperglycemia-induced endothelial dysfunction.
- To elucidate the role of F-box/LRR-repeat protein 7 (FBXL7) in the protective mechanism of 7ERM.
Main Methods:
- Human umbilical vein endothelial cells (HUVECs) were exposed to high glucose and varying doses of 7ERM.
- Cell injury, inflammation, reactive oxygen species (ROS) production, and FBXL7 expression were measured.
- FBXL7 was manipulated via siRNA knockdown and plasmid overexpression to assess its role.
Main Results:
- 7ERM treatment mitigated high glucose-induced cell injury, inflammation, and ROS production in HUVECs.
- High glucose increased FBXL7 expression, which was inhibited by 7ERM.
- FBXL7 knockdown protected against high glucose-induced cell injury, while its overexpression reduced 7ERM's protective effects.
Conclusions:
- 7-Ethoxyrosmanol (7ERM) effectively attenuates hyperglycemia-induced endothelial dysfunction in HUVECs.
- The protective mechanism involves the regulation of F-box/LRR-repeat protein 7 (FBXL7) expression.
- 7ERM demonstrates potential as a novel therapeutic drug for hyperglycemia treatment.
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