Published online by Cambridge University Press: 02 December 2014
It has been shown previously that S-100β levels in serum correspond with the severity of central nervous system (CNS) trauma. It also has been suggested that S-100β in CNS tissue is involved in neuroprotection and neuroregeneration. We have previously shown that administration of quercetin results in improved motor function in an animal model of spinal cord trauma.
Mid-thoracic spinal cord compression injury was produced in adult maleWistar rats. Serum and tissue samples were acquired from quercetin-treated animals (25 μmol / kg) and saline controls at 6, 12 and 24 hours after the trauma. S-100β levels were measured using a luminometric assay in the damaged tissue and in the serum of the animals.
The increase in serum S-100β levels seen in saline controls after spinal cord trauma was ameliorated in the quercetin-treated animals at all time points, although the difference to saline controls became statistically significant only at 24 hrs after the trauma. Compared to tissue S-100β levels in healthy animals, values were significantly decreased in saline controls at all three time points, while they were decreased at 6 hrs and increased at both 12 and 24 hrs in quercetin-treated animals. At all three time points tissue S-100β levels were significantly higher in quercetin-treated animals than in saline controls.
Administration of quercetin results in modification of S-100β levels in the setting of experimental spinal cord trauma. The kinetic patterns of the S-100β fluctuations in serum and tissue suggest that post-traumatic administration of quercetin decreases the extent of CNS injury.