Fig 1: EPO and VEGF proteins enhance the viability of bEnd.3 cells after OGD/R.An oxygen-glucose deprivation/reoxygenation (OGD/R) model was established in vitro. The bEnd. 3 cells were divided into 6 groups; control, OGD/R, VEGF, VEGF + PP1, EPO and EPO + PP1 groups. The control group did not experience OGD/R injury. The quantitative results of the cell viability in each group were obtained from three independent experiments. Data were expressed as mean ± SEM. ###P < 0.001 vs. control group; **P < 0.01, ***P < 0.001 vs. OGD/G group.
Fig 2: EA improved the expression of CD34, EPO, VEGF and p-Src proteins in the brain tissues of CIRI rats.(A) Representative blots showing the expression of CD34, EPO, VEGF and p-Src at different time points in the control, sham, model and EA groups. (B-E) Quantification of the expression level of CD34, EPO, VEGF and p-Src proteins (n = 5). Data were expressed as mean ± SEM. #P < 0.05, ##P < 0.01, ###P < 0.001 vs. sham group; *P < 0.05, **P < 0.01, ***P < 0.001 vs. model group.
Fig 3: The recombinant EPO protein increased the expression of VEGF and p-Src in bEnd.3 cells after OGD/R.(A) Representative expression of the VEGF and p-Src in the control, OGD/R, EPO, EPO + PP1 and EPO + XL184 groups. (B) Quantification of the expression level of VEGF and p-Src proteins (n = 5). Data were expressed as mean ± SEM. #P < 0.05 vs. control group; ***P < 0.001 vs. OGD/G group.
Fig 4: EA activated EPO mediated Src signaling pathway and VEGF signaling pathway to promote angiogenesis in CIRI rat brain tissue.EA at GV26 increased the expression of EPO in the brain tissue of CIRI rats and promoted angiogenesis by activating the downstream Src signaling pathway. In addition, the increased EPO enhanced the pro-angiogenesis effect of EA at GV26 by promoting the expression of VEGF.
Supplier Page from Sino Biological, Inc. for Mouse Erythropoietin / EPO Protein (His Tag)