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

Figure 3

Silymarin inhibited diabetes-induced proangiogenic response in brain endothelial cells. Advanced glycation end products (50 μg/mL) increased the migration rate of hBMECs. Treatment with silymarin inhibited AGE-induced brain endothelial cell migration in a dose-dependent manner. Representative images of the migrated cells (a) and a quantification of the migratory potential (b). Similarly, silymarin inhibited AGE-induced angiogenic response in human brain endothelial cells in a dose-dependent manner. Representative images of the tube formation potential of endothelial cells (c) and its quantification (d). Data are presented as mean ± SEM, . Significantly different as compared to control; ^$significantly different as compared to AGE; ^#significantly different as compared to AGE + 50 μg/mL-treated cells.

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