Silymarin Ameliorates Diabetes-Induced Proangiogenic Response in Brain Endothelial Cells through a GSK-3β Inhibition-Induced Reduction of VEGF Release

Figure 4

Silymarin inhibits diabetes-induced proangiogenic response in a GSK-3β inhibition-dependent reduction of VEGF release. Treatment with silymarin or GSK-3β inhibition using 10 nM of SB-216763 reduced AGE-induced migration in HBEC-5i. Cotreatment with both GSK inhibitor and silymarin resulted in a comparable inhibition to what is achieved in either of them (a). Treatment with AGE induced a onefold increase in VEGF release. This increase was blunted with silymarin cotreatment. GSK inhibition blunted AGE-induced VEGF release and did not alter silymarin-induced VEGF release inhibition (b). . Significantly different as compared to control; ^$significantly different as compared to AGE.

(a)

(b)