Hydroquinone shows neuroprotective potential in an experimental ischemic stroke model via attenuation of blood-brain barrier disruption
KeywordsIschemic Stroke Neuroprotective Effect Hydroquinone Post Treatment Focal Cerebral Ischemia
Hydroquinone (HQ), a major benzene metabolite, occurs naturally in various plants and food, and is also manufactured for commercial use. Although many studies have demonstrated the various biological effects of HQ, the neuroprotective effects of HQ following ischemic stroke have not been investigated. Therefore, in this study, we first examined the neuroprotective effects of HQ against ischemic damage in a focal cerebral ischemia rat model.
It was proven that pre and post treatment with 100 mg/ kg HQ protects from ischemia-induced cerebral damage, which was confirmed by evaluation of neurological deficit, positron-emission tomography and 2,3,5-triphenyltetrazoliumchloride staining.
In addition, pre and post treatment with 100 mg/kg HQ significantly attenuated ischemia-induced Evans blue dye extravasation, and significantly increased the immunoreactivities and protein levels of SMI-71 and glucose transporter-1 (GLUT-1), which were well known as useful makers of endothelial cells, in ischemic cortex compared with a vehicle-treated group.
Briefly, these results indicate that pre and post treatment with HQ can protect from ischemic damage induced by transient focal cerebral ischemia, and the neuroprotective effects of HQ may be closely associated with the prevention of BBB disruption via increase of SMI-71 and GLUT-1 expressions.
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