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Revascularization is necessary in patients with ischemic stroke, however it does not address inflammation that contribute to reperfusion injury and the early growth of ischemic core. We investigated EF24, an anti-inflammatory agent, in a stroke model. Ischemic stroke was induced in mice by occluding middle cerebral artery for 1 h followed by reperfusion. EF24 was given either 10 min post-reperfusion (EF24 Post ) or 10 min before occlusion (prophylactic, EF24 Pro ). Survival, ipsilateral uptake of radioactive infarct marker  18 F-fluoroglucaric acid (FGA), inflammatory cytokines, and tetrazolium chloride (TTC) staining were assessed. Survival was increased in both EF24-treated groups compared to the stroke+vehicle group. Ipsilateral  18 F-FGA uptake increased 2.6-fold in stroke+vehicle group compared to sham group ( p  &lt; 0.05); the uptake in EF24-treated groups and sham group was not significantly different. TTC-staining also showed reduction in infarct size by EF24 treatment. Plasma IL-6, TNF-α, and corticosterone did not show significant changes among groups. However, ipsilateral tissue in stroke+vehicle mice showed increased IL-6 (&gt;90-fold) and TNF-α (3-fold); the tissue IL-6 and TNF-α were significantly reduced in stroke+EF24 Pro  and stroke+EF24 Post  groups.  18 F-FGA uptake significantly correlated with tissue IL-6 levels. EF24 controls infarct growth and suppresses tissue inflammation in ischemic stroke, which can be monitored by  18 F-FGA uptake.

Evaluation of anti-inflammatory diphenyldihaloketone EF24 in transient ischemic stroke model