Figure 3
Pantoprazole induced angiogenic factors related to HO-1 induction. (A) RT-PCR and western blot for VEGF. Significant inductions of VEGF were noted with pantoprazole, significantly after 300 μM pantoprazole (p<0.05). These figures are representatives of the results obtained in 3 independent experiments. (B) The changes of VEGF and HO-1 with pantoprazole alone or combination of pantoprazole and ZnPPIX. The induction of VEGF after pantoprazole was significantly attenuated with HO-1 inhibitor, signifying the implication of HO-1 in PPI-induced VEGF. These figures are representatives of the results obtained in 3 independent experiments. (C) Other angiogenic factors related to pantoprazole. bFGF and VEGF was increasingly expressed with pantoprazole, but these inductions were attenuated with HO-1 inhibitor. These figures are representatives of the results obtained in 3 independent experiments. (D) in vitro angiogenesis assay. Tube formation of HUVEC was significantly decreased with 50 μM indomethacin. Pantoprazole compensated indomethacin-induced defective angiogenesis as assessed with the percentage of tube formation, whereas HO-1 inhibitor cancelled these overcome of pantoprazole-induced angiogenesis. These figures are representatives of the results obtained in 3 independent experiments.