Neuroprotection following fluid percussion brain trauma: a pilot study using quercetin

Previously, we were able to demonstrate the neuroprotective effect of quercetin in an animal model of acute traumatic spinal cord injury. The objective of the present study was to determine whether any neuroprotective effect is seen when quercetin is administered in an animal model of traumatic brain injury. Twenty-six adult male Sprague-Dawley rats were submitted to moderate fluid percussion injury in the anterior midline position. Animals were divided into two experimental groups: one group received 25 mumol/kg quercetin starting 1 h after injury, while animals in the second group received saline vehicle (n = 13 per group). Eight animals were used as uninjured healthy controls. Eight animals in each experimental group were sacrificed at 24 h, while five animals per group were allowed to recover for 72 h following injury. Compound action potential amplitudes (CAPAs) were recorded on 400-microm vibrotome sections of the corpus callosum superfused with oxygenated artificial CSF (n = 3 per animal) in 20 experimental animals and five healthy controls. Three brains from animals in each experimental group and healthy controls were used for histological, immunocytochemical and biochemical analysis after sacrifice at 24 h. CAPAs in uninjured animals had a mean of 1.12 mV. This decreased to 0.55 mV in saline vehicle-treated injured animals by 24 h and changed little over the next 3 days. CAPAs were significantly better at 0.82 mV at 24 h and 0.76 mV at 3 days in quercetin-treated injured animals when compared to injured saline vehicle controls. Quercetin significantly prevented decrease of glutathione levels and decreased myeloperoxidase activity. We conclude that this dietary flavonoid has therapeutic potential following brain trauma.