title: Bradykinin postconditioning protects pyramidal CA1 neurons against delayed neuronal death in rat hippocampus.
abstract: OBJECTIVE
  The present study was undertaken to evaluate possible neuroprotective effect of bradykinin against delayed neuronal death in hippocampal CA1 neurons if applied two days after transient forebrain ischemia in the rat.
  
  
  METHODS
  Transient forebrain ischemia was induced in male Wistar rats by four-vessel occlusion for 8 min. To assess efficacy of bradykinin as a new stressor for delayed postconditioning we used two experimental groups of animals: ischemia 8 min and 3 days of survival, and ischemia 8 min and 3 days of survival with i.p. injection of bradykinin (150 microg/kg) applied 48 h after ischemia.
  
  
  RESULTS
  We found extensive neuronal degeneration in the CA1 region at day 3 after ischemia/reperfusion. The postischemic neurodegeneration was preceded by increased activity of mitochondrial enzyme MnSOD in cytoplasm, indicating release of MnSOD from mitochondria in the process of delayed neuronal death. Increased cytosolic cytochrome c and subsequently caspase-3 activation are additional signs of neuronal death via the mitochondrial pathway. Bradykinin administration significantly attenuated ischemia-induced neuronal death, and also suppressed the release of MnSOD, and cytochrome c, and prevented caspase-3 activation.
  
  
  CONCLUSIONS
  Bradykinin can be used as an effective stressor able to prevent mitochondrial failure leading to apoptosis-like delayed neuronal death in postischemic rat hippocampus.
authors.affiliation: Institute of Neurobiology, Slovak Academy of Sciences, Kosice, Slovak Republic. danielis@saske.sk
authors.forename: Viera
authors.initials: V
authors.lastname: Danielisová
authors.forename: Miroslav
authors.initials: M
authors.lastname: Gottlieb
authors.forename: Miroslava
authors.initials: M
authors.lastname: Némethová
authors.forename: Petra
authors.initials: P
authors.lastname: Kravcuková
authors.forename: Iveta
authors.initials: I
authors.lastname: Domoráková
authors.forename: Eva
authors.initials: E
authors.lastname: Mechírová
authors.forename: Jozef
authors.initials: J
authors.lastname: Burda
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001920:Bradykinin / Q000627:therapeutic use*; D001921:Brain / Q000098:blood supply / Q000201:enzymology / Q000473:pathology; D053148:Caspase 3 / Q000378:metabolism; D002452:Cell Count; D016923:Cell Death / Q000187:drug effects; D045304:Cytochromes c / Q000378:metabolism; D006624:Hippocampus / Q000201:enzymology* / Q000473:pathology*; D007150:Immunohistochemistry; D002546:Ischemic Attack, Transient / Q000150:complications / Q000473:pathology*; D008297:Male; D009410:Nerve Degeneration / Q000209:etiology / Q000473:pathology*; D009474:Neurons / Q000201:enzymology*; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D045304:Cytochromes c; D013482:Superoxide Dismutase; D053148:Caspase 3; D001920:Bradykinin