Figure 6
From: DCZ19931, a novel multi-targeting kinase inhibitor, inhibits ocular neovascularization
DCZ19931 inhibits ocular neovascularization through p38-MAPK and ERK1/2-MAPK signaling. (A) The drug-target-disease network diagram of DCZ19931 involved in ocular neovascularization. (B) PPI network analysis. (C) GO enrichment analysis. (D) KEGG pathways enrichment analysis. (E) HUVECs were treated with DCZ19931 (500 nM), Ranibizumab (250 μg/mL), DCZ19931 (500 nM) plus Ranibizumab (250 μg/mL), or left untreated (Ctrl). Then, HUVECs were stimulated with or without VEGF (50 ng/mL) for 30 min. The expression levels of total ERK1/2, p38, JNK, p-ERK1/2, p-p38, and p-JNK were detected by western blots (n = 4). (F) HUVECs were treated with DCZ19931 (500 nM) or SB203580 (5 μmol/mL) plus U0126 (5 μmol/mL) for 24 h, and then stimulated with VEGF (50 ng/mL) for 30 min. The group without any treatment was taken as the control (Ctrl). The phosphorylated levels of ERK1/2 and p38 proteins were detected by western blots (n = 4). GAPDH was detected as the internal control. Representative immunoblots along with the densitometric quantitative results were shown. Statistical significance was determined by one-way ANOVA followed by Bonferroni post hoc test. *P < 0.05 indicated significant difference between the marked groups.
