title: The protection by octreotide against experimental ischemic stroke: up-regulated transcription factor Nrf2, HO-1 and down-regulated NF-κB expression.
abstract: BACKGROUND
  Inflammatory and oxidative damage play a pivotal role in cerebral ischemic pathogenesis and may represent a therapeutic target. Octreotide (OCT) has been proved to elicit a variety of biological effects through its anti-inflammatory and anti-oxidant properties in the treatment of severe acute pancreatitis and ischemia-reperfusion injury in retina and intestine. However little is known regarding the effect of OCT in ischemic stroke. Here, we designed this study to investigate the protective effect of OCT in ischemic stroke and explore the potential underlying mechanisms.
  
  
  METHODS
  Male Sprague-Dawley rats were subjected to permanent middle cerebral artery occlusion (pMCAO) and randomly divided into four groups: Sham (sham-operated), MCAO (pMCAO+0.9% saline), OCT-L (pMCAO+OCT 50μg/kg) and OCT-H (pMCAO+OCT 100μg/kg) groups. OCT was administered intraperitoneally immediately after stroke. Neurological deficit scores, infarct volume and brain water content were measured at 24h after stroke. Immunohistochemical staining and western blot were used to analyze the expressions of Nrf2, HO-1 and NF-κB. SOD and MDA were measured by spectrophotometer.
  
  
  RESULTS
  Compared with MCAO group, OCT significantly alleviated neurological deficit, lessened infarct volume and brain edema (P<0.05), upregulated the expression of Nrf2, HO-1 and SOD (P<0.05), and decreased the expression of NF-κB and MDA (P<0.05).
  
  
  CONCLUSIONS
  OCT protected the brain against cerebral ischemic damage; this effect may be through upregulation of transcription factor Nrf2, HO-1 and downregulation of NF-κB expression.
authors.affiliation: Department of Neurology, Second Hospital of Hebei Medical University; Shijiazhuang, Hebei 050000, PR China.
authors.forename: Linyu
authors.initials: L
authors.lastname: Chen
authors.forename: Lina
authors.initials: L
authors.lastname: Wang
authors.forename: Xiangjian
authors.initials: X
authors.lastname: Zhang
authors.forename: Lili
authors.initials: L
authors.lastname: Cui
authors.forename: Yinxue
authors.initials: Y
authors.lastname: Xing
authors.forename: Lipeng
authors.initials: L
authors.lastname: Dong
authors.forename: Zongjie
authors.initials: Z
authors.lastname: Liu
authors.forename: Yanhua
authors.initials: Y
authors.lastname: Li
authors.forename: Xiaolin
authors.initials: X
authors.lastname: Zhang
authors.forename: Chaohui
authors.initials: C
authors.lastname: Wang
authors.forename: Xue
authors.initials: X
authors.lastname: Bai
authors.forename: Jian
authors.initials: J
authors.lastname: Zhang
authors.forename: Lan
authors.initials: L
authors.lastname: Zhang
authors.forename: Xumeng
authors.initials: X
authors.lastname: Zhao
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism* / Q000517:prevention & control; D015536:Down-Regulation / Q000187:drug effects / Q000502:physiology; D005786:Gene Expression Regulation; D051547:Heme Oxygenase-1 / Q000096:biosynthesis*; D008297:Male; D051267:NF-E2-Related Factor 2 / Q000096:biosynthesis*; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000096:biosynthesis*; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use; D015282:Octreotide / Q000494:pharmacology / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020521:Stroke / Q000378:metabolism* / Q000517:prevention & control; D014157:Transcription Factors / Q000096:biosynthesis; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology
chemical_list: D051267:NF-E2-Related Factor 2; D016328:NF-kappa B; D018696:Neuroprotective Agents; C495637:Nfe2l2 protein, rat; D014157:Transcription Factors; D051547:Heme Oxygenase-1; D015282:Octreotide