title: HspB8 expression in brain tissue after cerebral ischemic reperfusion and atorvastatin intervention in Sprague-Dawley rats.
abstract: OBJECTIVE
  The aim of this study was to evaluate the expression of HspB8 in the brain cortex of Sprague-Dawley rats after cerebral ischemic reperfusion (I/R) and atorvastatin intervention. It also aimed to determine the possible mechanism of atorvastatin intervention. A model of cerebral I/R in Sprague-Dawley rats was used.
  
  
  METHODS
  Fifty-two male Sprague-Dawley rats were randomly divided into four groups. The normal and sham-operated groups received no treatment. The I/R group was intragastrically administered with physiological saline, and the intervention group received atorvastatin (10 mg/kg) prepared with physiological saline according to reperfusion time (time of palinesthesia, 24 and 48 hours). All rats were killed after 72 hours of reperfusion.
  
  
  RESULTS
  2,3,5-Triphenyltetrazolium chloride staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling showed that atorvastatin significantly reduced the volume of cerebral infarction (%) in the brain tissue and attenuated neuronal apoptosis in the cortex of rats, respectively. HspB8 was expressed in the pallium of Sprague-Dawley rats in the normal and sham-operated groups. The expression level of HspB8 was significantly upregulated after cerebral I/R. However, the level of HspB8 expressed was lower in the intervention group than in the I/R group.
  
  
  CONCLUSIONS
  The expression of HspB8 was upregulated after cerebral I/R injury. Atorvastatin affected the precursors of the heat shock stress response, relieved stress injury due to cerebral ischemia, downregulated HspB8 expression, and inhibited nerve cell apoptosis in the brain cortex. However, HspB8 might not contribute to atorvastatin-mediated cytoprotective effects.
authors.forename: Xi
authors.initials: X
authors.lastname: Tao
authors.forename: Wei
authors.initials: W
authors.lastname: Lu
authors.forename: Jinggui
authors.initials: J
authors.lastname: Deng
authors.forename: Zhiping
authors.initials: Z
authors.lastname: Hu
authors.forename: Qiang
authors.initials: Q
authors.lastname: Lei
authors.forename: Jinnan
authors.initials: J
authors.lastname: Zhang
authors.forename: Tao
authors.initials: T
authors.lastname: Song
authors.forename: Jia
authors.initials: J
authors.lastname: Liu
authors.forename: Lijun
authors.initials: L
authors.lastname: Zheng
authors.forename: Juan
authors.initials: J
authors.lastname: He
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D000069059:Atorvastatin; D015153:Blotting, Western; D002545:Brain Ischemia / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D002540:Cerebral Cortex / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D006360:Heat-Shock Proteins / Q000378:metabolism*; D006538:Heptanoic Acids / Q000494:pharmacology*; D020287:In Situ Nick-End Labeling; D020244:Infarction, Middle Cerebral Artery; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D011758:Pyrroles / Q000494:pharmacology*; D011897:Random Allocation; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D012720:Severity of Illness Index; D013778:Tetrazolium Salts
chemical_list: D006360:Heat-Shock Proteins; D006538:Heptanoic Acids; C490753:HspB8 protein, rat; D018696:Neuroprotective Agents; D011758:Pyrroles; D013778:Tetrazolium Salts; C009591:triphenyltetrazolium; D000069059:Atorvastatin
keywords: Apoptosis,; Atorvastatin,; Cerebral ischemia/reperfusion,; HspB8,; Volume of cerebral infarction