Figure 5. DV neuroprotection is VEGF and VEGFR mediated.

(A) Anti-VEGF Western blot analysis of ipsilateral stroke hemispheres as labeled, with GAPDH as internal loading control. (B) Densitometry analysis of VEGF Western blot as shown in A as normalized to corresponding GAPDH bands (**P < 0.01, n = 15 per treatment group, per PSD). (C) Plot of VEGF ELISA ipsilateral stroke brain tissue treated as labeled (^#P < 0.01 as compared with corresponding PBS-treated WT control or as labeled, n = 3 per treatment group per PSD). (D) Mean ischemic lesion volumes of stroke WT mice on PSD 1–3 treated as labeled (**P < 0.01, n = 15 per treatment group per PSD). (E) Vibrissae-elicited forelimb placement test on WT mice treated as labeled. DV had no effect in animals also treated with PTK787/ZK 222584 (P = NS). (F) NeuN and VEGFR2 co-immunohistochemistry of PSD 5 peri-infarct brain tissue of mice treated as labeled. White arrows indicate cells that were positive for both NeuN and VEGFR2. Scale bar: 50 μm. (G) Number of NeuN- and VEGFR2-positive cells per mm² in the peri-infarct regions as labeled (**P < 0.01, n = 10 images per animal, 5 animals per treatment condition).