title: Occlusion of middle cerebral artery induces apoptosis of cerebellar cortex neural cells via caspase-3 in rats.
abstract: OBJECTIVE
  Occlusion of the middle ferebral artery in rats may cause secondary injury     that is not associated with middle ferebral artery feeding zone. This entity has     been investigated very rarely.
  
  
  METHODS
  HE staining method observed     the changes of cerebellar cortex after MCAO operation. Electron Microscopy and     TUNEL methods observed the apoptosis of neural cells of cerebellar cortex after     MCAO in rats. Immunohistochemical analyses method observed the caspase-3 in     neural cells of cerebellar cortex.
  
  
  RESULTS
  The results of HE staining indicated     that no ischemia-necrosis changes of cerebellar cortex tissue were observed     after MCAO operation by HE staining. Further experiments by Electron Microscopy     and TUNEL assay revealed that the apoptosis of neural cells of cerebellar cortex     were induced after MCAO in rats. Furthermore, immunohistochemical analyses     showed that caspase-3 played an important role on MCAO-induced apoptosis of     neural cells of cerebellar cortex.
  
  
  CONCLUSIONS
  These data showed for the first     time that the role of caspase-3 in the mechanism of secondary injury of     separated infarction in cerebellar cortex after middle cerebral artery occlusion     in rats and it might give a new treatment strategy for individuals with human     ischemic stroke.
authors.affiliation: China Medical University the Fourth Affiliated Hospital, Department of Neurology, Shenyang, China.
authors.forename: Li
authors.initials: L
authors.lastname: Jie
authors.forename: Che
authors.initials: C
authors.lastname: Yuqin
authors.forename: Diao
authors.initials: D
authors.lastname: Yao
authors.forename: Hou
authors.initials: H
authors.lastname: Shuai
authors.forename: Wang
authors.initials: W
authors.lastname: Yuanyuan
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D051017:Apoptosis Regulatory Proteins / Q000502:physiology; D020520:Brain Infarction / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology*; D053148:Caspase 3 / Q000502:physiology*; D002525:Cerebellar Cortex / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology*; D002526:Cerebellar Diseases / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D020287:In Situ Nick-End Labeling / Q000379:methods; D020244:Infarction, Middle Cerebral Artery / Q000150:complications / Q000503:physiopathology*; D008854:Microscopy, Electron / Q000379:methods; D009410:Nerve Degeneration / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology; D009474:Neurons / Q000201:enzymology / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction / Q000502:physiology
chemical_list: D051017:Apoptosis Regulatory Proteins; C505410:Casp3 protein, rat; D053148:Caspase 3