Scutellarin Prevents Angiogenesis in Diabetic Retinopathy by Downregulating VEGF/ERK/FAK/Src Pathway Signaling

Figure 2

SCU inhibited glucose/CoCl2-induced HREC proliferation, migration, and tube formation. (a) HRECs were treated with SCU (10 μm/l), glucose (30 mm/l), and CoCl₂ (200 μm/l) as the graph showed for 0 h, 24 h, 48 h, or 72 h, and cell survival rate was determined using the CCK-8 assay. Cell proliferation was calculated as a percentage of the control. Data are presented as (). compared to the control group, the osmotic control group, the SCU group, and the SCU+glucose/CoCl₂ group. ^# compared to the glucose+CoCl₂ group. The control, osmotic control, and SCU groups have no statistical significance (). (b) The results of transwell assay, wound healing assay, and Matrigel tubulogenesis assay.  μm. (c) The quantitative results of HRECs migrated of transwell assay is measured by a microplate reader. (d) Scratched areas, which were not covered by migrated cells, were measured using ImageJ (NIH) for the quantification. (e–g) The images of Matrigel tubulogenesis assay were quantified as the number of junctions, number of tubules, and total tubule length. Images were processed using Adobe Photoshop CS2 9.0.2 (Adobe Systems, San Jose, CA) with the Image Processing Tool Kit plug-ins (Reindeer Graphics, Asheville, NC) and analyzed using AngioSys 1.0 (TCS Cellworks, Buckingham, England). All the data in (c)–(g) were presented as ; compared to the control group, the osmotic control group, and the SCU+glucose+CoCl₂ group; ^# compared to the control group, the osmotic control group, and the glucose+CoCl₂ group.

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