VEGF induced hyperpermeability in bovine aortic endothelial cell and inhibitory effect of salvianolic acid B
Abstract
Aim: To examine the effect of recombinant human vascular endothelial growth factor (VEGF) on the low density lipoprotein (LDL) permeability of bovine aortic endothelial cells (BAEC) and the inhibitory effect of salvianolic acid B in vitro.
Methods: The confluence BAEC monolayers were cultured with normal medium and with medium containing VEGF or salvianolic acid B at various concentrations and for various time periods. The iodine labeled LDL flux across the monolayers was then performed, and radioactivity was measured by SN-695 automatic liquid scintillation counter.
Results: Addition of purified human recombinant VEGF to the BAEC monolayers could significantly increase the permeability of the monolayer to 125I-LDL (P < 0.01). The permeability-increasing activity of VEGF on the BAEC monolayers was both dose and time dependent. Salvianolic acid B could markedly inhibit the VEGF-induced hyperpermeability in BAECs (P < 0.01).
Conclusion: VEGF plays a role in the formation and development of atherosclerosis, and salvianolic acid B has inhibitory effect on VEGF-induced hyperpermeability in BAEC.
Keywords:
Methods: The confluence BAEC monolayers were cultured with normal medium and with medium containing VEGF or salvianolic acid B at various concentrations and for various time periods. The iodine labeled LDL flux across the monolayers was then performed, and radioactivity was measured by SN-695 automatic liquid scintillation counter.
Results: Addition of purified human recombinant VEGF to the BAEC monolayers could significantly increase the permeability of the monolayer to 125I-LDL (P < 0.01). The permeability-increasing activity of VEGF on the BAEC monolayers was both dose and time dependent. Salvianolic acid B could markedly inhibit the VEGF-induced hyperpermeability in BAECs (P < 0.01).
Conclusion: VEGF plays a role in the formation and development of atherosclerosis, and salvianolic acid B has inhibitory effect on VEGF-induced hyperpermeability in BAEC.