title: Effects of lecithinized superoxide dismutase on neuronal cell loss in CA3 hippocampus after traumatic brain injury in rats.
abstract: BACKGROUND
  The protective effect of excitatory amino acid antagonists for CA3 hippocampal neuronal loss has been well documentated. From a clinical point of view, however, alternative therapies should also be explored because excitatory amino acid antagonists have relatively deleterious side effects. Administration of lecithinized superoxide dismutase (PC-SOD) has recently been demonstrated to reduce brain edema after traumatic brain injury (TBI) in the cerebral cortex. In this study, we investigated the effectiveness of PC-SOD on CA3 hippocampal cell loss by examining hematoxylin and eosin-stained sections.
  
  
  METHODS
  Rats were divided at random into three groups. The first group received 1 mL of saline (contusion + saline group, n = 5). Rats of the second group were treated with 3000 IU/kg of PC-SOD (contusion + SOD 1 group, n = 5), while the third group received 5000 IU/kg of PC-SOD (contusion + SOD 2 group, n = 5). All agents were administered intraperitoneally 1 minute after traumatic insult and every 24 hours until 2 or 3 days post-TBI. Animals were sacrificed 3 or 7 days after contusion injury.
  
  
  RESULTS
  PC-SOD prevented CA3 neuronal loss 3 days after TBI, and increased the number of surviving CA3 neurons 7 days after TBI.
  
  
  CONCLUSIONS
  Our findings suggest that PC-SOD may serve as a pharmacological agent in the treatment of neuronal loss after TBI.
authors.affiliation: Department of Neurological Surgery, Okayama University Medical School, 2-5-1 Shikata-cho, Okayama 700, Japan.
authors.forename: Masatoshi
authors.initials: M
authors.lastname: Yunoki
authors.forename: Masamitsu
authors.initials: M
authors.lastname: Kawauchi
authors.forename: Naoya
authors.initials: N
authors.lastname: Ukita
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Sugiura
authors.forename: Takashi
authors.initials: T
authors.lastname: Ohmoto
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000150:complications* / Q000188:drug therapy* / Q000473:pathology; D002452:Cell Count; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D006624:Hippocampus / Q000187:drug effects* / Q000293:injuries* / Q000473:pathology; D008297:Male; D009410:Nerve Degeneration / Q000209:etiology* / Q000473:pathology / Q000517:prevention & control*; D010713:Phosphatidylcholines / Q000008:administration & dosage / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000008:administration & dosage / Q000627:therapeutic use*; D013997:Time Factors
chemical_list: D010713:Phosphatidylcholines; D013482:Superoxide Dismutase; C434045:lecithinized superoxide dismutase