Emerging evidence suggests that aryl hydrocarbon receptor (AhR) antagonism could attenuate neuronal damage caused by transient ischemic stroke. However, the optimal timing of AhR antagonist administration for maximum neuroprotective efficacy has yet to be established. The present study explored this issue via MRIs in rats with transient ischemic stroke and demonstrated that infarct volume and apoptosis were alleviated in rats that received AhR antagonists 10 or 50 minutes after ischemia. In addition, the timing of AhR antagonist administration was shown to affect edema formation caused by transient ischemic stroke.
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