Calcium dobesilate may alleviate diabetes‑induced endothelial dysfunction and inflammation

Area of Science:

• Nephrology
• Endocrinology
• Pharmacology

Background:

• Diabetic kidney disease (DKD) is a major cause of end-stage renal disease with unclear pathogenesis.
• Effective treatments for DKD are lacking, necessitating research into underlying mechanisms and therapeutic strategies.

Purpose of the Study:

• To investigate the effects of high glucose (HG) on human umbilical vein endothelial cells (HUVECs).
• To evaluate the potential of calcium dobesilate (CaD) in protecting HUVECs against HG-induced damage and inflammation.

Main Methods:

• HUVECs were exposed to varying D-glucose concentrations and calcium dobesilate (CaD).
• Cell proliferation (Cell Counting Kit-8), angiogenesis (migration assays, FITC-BSA permeability), and expression of endothelial dysfunction and inflammation markers (VEGF, VEGFR, endocan, ICAM-1, MCP-1, PTX3) were assessed using RT-qPCR and Western blotting.

Main Results:

• High glucose (HG) increased HUVEC proliferation, migration, and permeability, while upregulating markers of endothelial dysfunction and inflammation.
• CaD treatment inhibited HG-induced HUVEC proliferation and migration.
• CaD prevented HG-induced increases in FITC-BSA permeability and suppressed the overexpression of endothelial and inflammation markers.

Conclusions:

• CaD exhibits angioprotective properties by ameliorating HG-induced inflammation in endothelial cells.
• CaD demonstrates potential therapeutic applicability for diabetic nephropathy, especially in early stages.