title: Brain edema after intracerebral hemorrhage in rats: the role of inflammation.
abstract: BACKGROUND
  Intracerebral hemorrhage (ICH) results in secondary brain edema and injury that may lead to death and disability. ICH also causes inflammation. It is unclear whether inflammation contributes to brain edema and neuron injury or functions in repairing the brain tissue.
  
  
  OBJECTIVE
  To understand the effect of inflammation in ICH, we have carried out an investigation on the various aspects and the dynamic changes of inflammation.
  
  
  METHODS
  An ICH model was generated by injecting 50 microl autologous tail artery blood stereotactically into the right caudate nucleus of 30 rats, which were randomly divided into five ICH groups. Similarly, five Sham control groups were generated by inserting the needle to the right caudate nucleus of rats.
  
  
  METHODS
  Rat behavior was evaluated over the time course (6 h, 24 h, 48 h, 72 h and 7 d) in each group. The rats were then killed by administering an overdose of pentobarbital. Following the euthanasia, the brain water content, neuronal loss, glia proliferation, inflammatory infiltration and brain morphology of the rats were measured. Additionally, the expression of TNF-alpha, IL-6, ICAM-1, VEGF, NF-kappaB, C3 and CR2 was analyzed by immunohistochemistry.
  
  
  METHODS
  The data were analyzed by student's t test.
  
  
  RESULTS
  Rat brain water content increased progressively over the time course and reached its peak at 48 h followed ICH. The maximum of inflammatory infiltrate (especially neutrophils) and immunopositive cells of TNF-alpha, IL-6 and NF-kappaB, were at 48 h. The expression of C3 and CR2 reached their peaks at 48-72 h, while the expression ICAM-1 and VEGF were at maximum at 72 h followed ICH.
  
  
  CONCLUSIONS
  The results suggested that the inflammatory cytokines, complement system and VEGF may have a function in the development of the brain edema and neuron injury followed ICH.
authors.affiliation: Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, China.
authors.forename: Xiangjian
authors.initials: X
authors.lastname: Zhang
authors.forename: Haiyan
authors.initials: H
authors.lastname: Li
authors.forename: Shuchao
authors.initials: S
authors.lastname: Hu
authors.forename: Liying
authors.initials: L
authors.lastname: Zhang
authors.forename: Chunyan
authors.initials: C
authors.lastname: Liu
authors.forename: Chunhua
authors.initials: C
authors.lastname: Zhu
authors.forename: Ruichun
authors.initials: R
authors.lastname: Liu
authors.forename: Chunyan
authors.initials: C
authors.lastname: Li
mesh_terms: D000818:Animals; D001929:Brain Edema / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D002543:Cerebral Hemorrhage / Q000150:complications / Q000276:immunology* / Q000473:pathology; D003176:Complement C3 / Q000096:biosynthesis; D007249:Inflammation; D018836:Inflammation Mediators / Q000378:metabolism*; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D008297:Male; D023421:Models, Animal; D016328:NF-kappa B / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D017464:Receptors, Complement 3d / Q000096:biosynthesis; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis
chemical_list: D003176:Complement C3; D018836:Inflammation Mediators; D015850:Interleukin-6; D016328:NF-kappa B; D017464:Receptors, Complement 3d; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; D018799:Intercellular Adhesion Molecule-1