Silicon-based agent attenuates cerebral ischemia-reperfusion injury in a rat model.

Cerebral ischemia-reperfusion (IR) injury is a major cause of brain damage following stroke, in which excessive reactive oxygen species play a critical role. Therefore, the development of novel therapeutic agents targeting oxidative stress is highly desirable. We investigated the protective effects of an orally administered silicon (Si)-based agent that continuously generates hydrogen in the intestinal tract, thereby acting as a selective antioxidant, in a rat model of middle cerebral artery occlusion and reperfusion. Rats fed an Si-based agent-containing diet showed trends toward improved neurological symptom scores, reduced asymmetric behavior in the elevated body swing test, and a higher survival rate compared with control rats. Furthermore, infarct size was significantly reduced in the Si group. Analysis of plasma derivatives of reactive oxygen metabolites revealed a significant reduction in systemic oxidative stress in the Si group. These results suggest that the Si-based agent exerts protective effects against cerebral IR injury, at least in part through its antioxidant effects, warranting further preclinical investigation.