title: Neuroprotective effect of levetiracetam on hypoxic ischemic brain injury in neonatal rats.
abstract: OBJECTIVE
  Hypoxic-ischemic brain injury that occurs in the perinatal period is one of the leading causes of mental retardation, visual and auditory impairment, motor defects, epilepsy, cerebral palsy, and death in neonates. The severity of apoptosis that develops after ischemic hypoxia and reperfusion is an indication of brain injury. Thus, it may be possible to prevent or reduce injury with treatments that can be given before the reperfusion period following hypoxia and ischemia. Levetiracetam is a new-generation antiepileptic drug that has begun to be used in the treatment of epilepsy.
  
  
  METHODS
  The present study investigated the effects of levetiracetam on neuronal apoptosis with histopathological and biochemical tests in the early period and behavioral experiments in the late period.
  
  
  RESULTS
  This study showed histopathologically that levetiracetam reduces the number of apoptotic neurons and has a neuroprotective effect in a neonatal rat model of hypoxic-ischemic brain injury in the early period. On the other hand, we demonstrated that levetiracetam dose dependently improves behavioral performance in the late period.
  
  
  CONCLUSIONS
  Based on these results, we believe that one mechanism of levetiracetam's neuroprotective effects is due to increases in glutathione peroxidase and superoxide dismutase enzyme levels. To the best of our knowledge, this study is the first to show the neuroprotective effects of levetiracetam in a neonatal rat model of hypoxic-ischemic brain injury using histopathological, biochemical, and late-period behavioral experiments within the same experimental group.
authors: Department of Pediatric Neurology, Mersin University School of Medicine, 33060, Zeytinlibahce, Mersin, Turkey, drmustafakomur@yahoo.com.
authors: Mustafa
authors: M
authors: Komur
authors: Cetin
authors: C
authors: Okuyaz
authors: Yalcin
authors: Y
authors: Celik
authors: Bora
authors: B
authors: Resitoglu
authors: Ayse
authors: A
authors: Polat
authors: Senay
authors: S
authors: Balci
authors: Lulufer
authors: L
authors: Tamer
authors: Semra
authors: S
authors: Erdogan
authors: Huseyin
authors: H
authors: Beydagi
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis / Q000187:drug effects; D001930:Brain Injuries / Q000097:blood / Q000209:etiology* / Q000473:pathology / Q000517:prevention & control*; D053148:Caspase 3 / Q000378:metabolism; D002374:Catalase / Q000097:blood; D002452:Cell Count; D004305:Dose-Response Relationship, Drug; D005979:Glutathione Peroxidase / Q000097:blood; D020925:Hypoxia-Ischemia, Brain / Q000150:complications*; D020287:In Situ Nick-End Labeling; D000077287:Levetiracetam; D008315:Malondialdehyde / Q000097:blood; D018782:Maze Learning / Q000187:drug effects; D009474:Neurons / Q000187:drug effects / Q000473:pathology; D018697:Nootropic Agents / Q000627:therapeutic use*; D010889:Piracetam / Q000031:analogs & derivatives* / Q000627:therapeutic use; D051381:Rats; D013482:Superoxide Dismutase / Q000097:blood; D013997:Time Factors
chemical_list: D018697:Nootropic Agents; D000077287:Levetiracetam; D008315:Malondialdehyde; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D053148:Caspase 3; D010889:Piracetam