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Cerebral ischemia is a major cause of death and disability worldwide, and treatments for it are limited. A new therapeutic strategy of brain protection after acute stroke targets the neurovascular unit, such as endothelial cells, astrocytes, microglia, and neurons, instead of neurons only (Fig. 1). Edaravone, a novel free radical scavenger, has been used to treat acute ischemic stroke in Japan. We have previously reported the antiedema effect of the combination therapy of edaravone and mild hypothermia at 35C following transient focal cerebral ischemia (tFCI). However, the mechanism of the effect remains unclear. In the present study, we tested the hypothesis that this combination therapy can reduce oxidative stress and the activation of matrix metalloproteinase-9 (MMP-9), which is related to blood-brain barrier (BBB) dysfunction, and brain edema formation after tFCI.

Neuroprotective Effect of an Antioxidant in Ischemic Stroke: Involvement of Neuronal Death Signaling and Blood-brain Barrier Disruption