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Ellagic acid and allopurinol decrease H 2 O 2 concentrations, epileptiform activity and astrogliosis after status epilepticus in the hippocampus of adult rats.

Kenia Pardo-PeñaAldo Yañez-HernándezLaura Medina-CejaAlberto Morales-Villagrán
Published in: Experimental brain research (2022)
Status epilepticus (SE) can result in an overproduction of hydrogen peroxide (H 2 O 2 ), which contributes to oxidative stress and brain injury during different phases of epileptogenesis and seizures. The purpose of this study was to evaluate the effects of ellagic acid and allopurinol administered after SE on H 2 O 2 concentrations, electrical activity and GFAP immunoreactivity in the hippocampus of rats evaluated on Day 18 after SE. H 2 O 2 levels were measured using an online technique with high temporal resolution and simultaneous electrical activity recording. For this purpose, the lateral ventricles of male Wistar rats (200-250 g) were injected with pilocarpine (2.4 mg/2 µl) to induce SE. After SE, rats were injected with ellagic acid (50 mg/kg i.p., and two additional doses at 24 and 48 h) or allopurinol (50 mg/kg i.p., single dose). Administration of ellagic acid or allopurinol after SE significantly reduced the H 2 O 2 concentrations and decreased the presence of epileptiform activity and GFAP immunoreactivity in the hippocampus 18 days after SE. In conclusion, the administration of antioxidants potentially reduces oxidative stress, which indicates the possible attenuation of the neurobiological consequences after SE.
Keyphrases
  • brain injury
  • oxidative stress
  • hydrogen peroxide
  • cerebral ischemia
  • subarachnoid hemorrhage
  • minimally invasive
  • single molecule
  • blood brain barrier
  • signaling pathway
  • ischemia reperfusion injury