title: Physical exercise induces expression of CD31 and facilitates neural function recovery in rats with focal cerebral infarction.
abstract: OBJECTIVE
  The present study was aimed at examining the role of physical exercise in the improvement of damaged neural function and the induction of angiogenesis.
  
  
  METHODS
  An infarction model was induced by ligating the left middle cerebral artery occlusion (MCAO) in a total of 66 adult Sprague-Dawley rats that were further randomly divided into three groups: the physical exercise group (n=30), which was given running wheel exercise every day after MCAO, the control group (n=30) and sham-operated group (n=6), which were fed in standard cages without any special training exercise. The rats were killed on the third, seventh and fourteenth days and the neurological severity scores were examined for evaluating the neural function. And the neogenetic microvessels around the peri-infarction region were checked with the specific marker CD31.
  
  
  RESULTS
  Although neogenetic microvessels in the peri-infarction region were observed in both control group and physical exercise group, which showed the highest signal on the seventh day after ischemia, the number of CD31 positive cells significantly increased in physical exercise group in comparison with those in control group on the seventh and fourteenth days after ischemia (p<0.01). Moreover, the neurological severity scores in the physical exercise group showed more quick declination as compared to those in control group from the seventh day after ischemic.
  
  
  CONCLUSIONS
  Our results suggested that physical exercise plays an important role in the recovery of damaged neural function and induction of angiogenesis after cerebral infarction in rats.
authors.affiliation: Department of Rehabilitation Medicine, Second Affiliated Hospital, Sun Yat-sen University, Guangzhou 510120, China.
authors.forename: Xiquan
authors.initials: X
authors.lastname: Hu
authors.forename: Haiqing
authors.initials: H
authors.lastname: Zheng
authors.forename: Tiebin
authors.initials: T
authors.lastname: Yan
authors.forename: Sanqiang
authors.initials: S
authors.lastname: Pan
authors.forename: Jie
authors.initials: J
authors.lastname: Fang
authors.forename: Ruishu
authors.initials: R
authors.lastname: Jiang
authors.forename: Shangfeng
authors.initials: S
authors.lastname: Ma
mesh_terms: D000818:Animals; D002452:Cell Count; D002544:Cerebral Infarction / Q000235:genetics / Q000473:pathology / Q000628:therapy*; D004185:Disability Evaluation; D004195:Disease Models, Animal; D008297:Male; D008833:Microcirculation / Q000235:genetics; D018919:Neovascularization, Physiologic / Q000235:genetics; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D010805:Physical Conditioning, Animal / Q000379:methods*; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000096:biosynthesis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function / Q000235:genetics*; D012720:Severity of Illness Index; D013997:Time Factors; D015533:Transcriptional Activation / Q000502:physiology*; D016896:Treatment Outcome
chemical_list: D019408:Platelet Endothelial Cell Adhesion Molecule-1