Fig. 1

anti-VCAM-CD39 is effective in mitigating brain damage following global forebrain hypoxia. (A) MRI-based DWI-quantified infarct volumes (mm³) of anti-VCAM-CD39 treated mouse brains 24 h post-DCAL showed significantly lower infarct volumes on the side of permanent occlusion compared to saline, non-targeted CD39 and anti-VCAM-inactive CD39 controls. (Data is Mean ± SEM; Saline: n = 5, anti-VCAM-CD39: n = 5; *p < 0.05; one-way ANOVA with Sidak’s post‐hoc analysis). (B) MR T2* imaging and Cresyl Violet histological staining of mouse brains post-DCAL after treatment with (i) saline, (ii) anti-VCAM-CD39, (iii) non-targeted CD39, (iv) anti-VCAM-inactive CD39 (n = 4–5) distinctly show the infarcted area indicated by delineation, and this injury and corresponding absence of Cresyl violet positive cells in the same region, indicated by the arrows, confirming cell death. (C) anti-VCAM-CD39 significantly reduced neurological score compared to saline, and also had lower scores compared to drug control groups (Saline: n = 19, anti-VCAM-CD39: n = 14–17; Bars indicate median value, **p < 0.01, ***p < 0.001; Kruskal Wallis test with Dunnett’s post‐hoc analysis).(D) Infarct volume correlates with Bederson scores (n = 10). (E) Caspase activity 24-hours post-DCAL is significantly increased in the site of permanent occlusion, and anti-VCAM-CD39 was able to significantly decrease apoptotic activity. (Data is Mean ± SEM; Saline: n = 13, anti-VCAM-CD39: n = 6–11; *p < 0.05, ***p < 0.001, ****p < 0.0001; two-way ANOVA with Uncorrected Fisher’s LSD). (F) BBB permeability measured by albumin extravasation in the brain parenchyma was significantly increased on the side of permanent occlusion post-DCAL, and anti-VCAM-CD39 treatment was effective in reducing albumin extravasation (Data is Mean ± SEM; Saline: n = 12, anti-VCAM-CD39: n = 12; *p < 0.05; one‐way ANOVA with Sidak’s post‐hoc analysis)