title: Ischemic postconditioning diminishes matrix metalloproteinase 9 expression and attenuates loss of the extracellular matrix proteins in rats following middle cerebral artery occlusion and reperfusion.
abstract: OBJECTIVE
  Ischemic postconditioning (IPostC) has been proved to have neuroprotective effects for cerebral ischemia, but the underlying mechanism remains elusive. This study aimed at validating the neuroprotective effects of IPostC and investigating whether the neuroprotection of IPostC is associated with matrix metalloproteinase 9 (MMP9) and the extracellular matrix proteins, laminin and fibronectin, following cerebral ischemia/reperfusion in rats.
  
  
  METHODS
  The rats in middle cerebral artery occlusion (MCAO) group underwent MCAO and reperfusion, and the animals in MCAO + IPostC group were treated by occluding bilateral common carotid arteries for 10 seconds and then reperfusing for 10 seconds for five episodes at the beginning of MCAO. Apoptosis was detected with terminal deoxynucleotidyl transferase dUTP nick end labeling staining. The expression of MMP9, laminin, and fibronectin was measured with immunofluorescence and enzyme-linked immunosorbent assay.
  
  
  RESULTS
  IPostC reduced brain edema and infarct volume and improved the neurological function. Furthermore, IPostC decreased cell apoptosis compared with the MCAO group. Compared to the MCAO group, IPostC treatment reduced MMP9 expression. Moreover, the results showed that the expression of laminin and fibronectin significantly increased in the MCAO + IPostC group compared to the MCAO group.
  
  
  CONCLUSIONS
  These findings indicated that diminishment of MMP9 expression and the attenuation of degradation of laminin and fibronectin may be involved in the protective mechanisms of postconditioning against cerebral ischemia/reperfusion injury.
authors.affiliation: Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, Key Laboratory of Neurodegenerative Diseases (Capital Medical University), Ministry of Education, Beijing, China.
authors.forename: Xiang-Rong
authors.initials: XR
authors.lastname: Liu
authors.forename: Mei
authors.initials: M
authors.lastname: Luo
authors.forename: Feng
authors.initials: F
authors.lastname: Yan
authors.forename: Chen-Cheng
authors.initials: CC
authors.lastname: Zhang
authors.forename: Si-Jie
authors.initials: SJ
authors.lastname: Li
authors.forename: Hai-Ping
authors.initials: HP
authors.lastname: Zhao
authors.forename: Xun-Ming
authors.initials: XM
authors.lastname: Ji
authors.forename: Yu-Min
authors.initials: YM
authors.lastname: Luo
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism; D001929:Brain Edema; D020520:Brain Infarction / Q000209:etiology; D004797:Enzyme-Linked Immunosorbent Assay; D005353:Fibronectins / Q000378:metabolism*; D015971:Gene Expression Regulation, Enzymologic / Q000502:physiology*; D020287:In Situ Nick-End Labeling; D020244:Infarction, Middle Cerebral Artery / Q000378:metabolism* / Q000473:pathology; D057775:Ischemic Postconditioning / Q000379:methods*; D007797:Laminin / Q000378:metabolism*; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
chemical_list: D005353:Fibronectins; D007797:Laminin; D020780:Matrix Metalloproteinase 9; C572337:Mmp9 protein, rat