title: Protective effects of pentoxifylline on the brain following remote burn injury.
abstract: BACKGROUND
  Brains are often subject to injurious effect following remote burn injury and increased productions of inflammatory cytokines are involved. It is also known that pentoxifylline (PTX) exerts multiple beneficial effects on the inflammatory cascade. Therefore, we investigated whether a single dose of PTX given immediately following severe remote burn would protect the brain from the injurious effects.
  
  
  METHODS
  Rats were divided randomly into the sham burn group, burn placebo-treated group and burn PTX-treated group. Single dose of PTX was injected 15 min following initial burn injury. We measured the levels of tumour necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-10 in the brain tissue at 0.5, 1, 2, 4, 8 and 16 h after burn. Other measures included the level of nuclear factor-kappaB (NF-κB) activation, glial activation and apoptosis of cortical cells.
  
  
  RESULTS
  PTX substantially suppressed the burn-induced surge in the levels of TNF-α, IL-1β, and IL-6 in the rat-brain tissues. PTX reduced the level of burn-induced apoptosis. PTX also significantly reduced the activation of nuclear transcription factor NF-κB and reduced the activation of glial cells in the brain tissue.
  
  
  CONCLUSIONS
  An early, single dose of PTX dramatically reduced brain inflammation and apoptosis for up to 16 h post-injury.
authors.affiliation: Department of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, 305 East Zhongshan Road, Nanjing 210002, PR China.
authors.forename: Qing
authors.initials: Q
authors.lastname: Ji
authors.forename: Hongbin
authors.initials: H
authors.lastname: Jia
authors.forename: Haibin
authors.initials: H
authors.lastname: Dai
authors.forename: Weiyan
authors.initials: W
authors.lastname: Li
authors.forename: Lidong
authors.initials: L
authors.lastname: Zhang
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D017209:Apoptosis / Q000502:physiology; D015415:Biomarkers / Q000378:metabolism; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D002056:Burns / Q000150:complications* / Q000188:drug therapy / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D007150:Immunohistochemistry; D007249:Inflammation / Q000378:metabolism / Q000473:pathology; D008297:Male; D016328:NF-kappa B / Q000378:metabolism; D009419:Nerve Tissue Proteins / Q000032:analysis; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D010431:Pentoxifylline / Q000627:therapeutic use*; D010726:Phosphodiesterase Inhibitors / Q000627:therapeutic use*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D016207:Cytokines; D016328:NF-kappa B; D009419:Nerve Tissue Proteins; D018696:Neuroprotective Agents; D010726:Phosphodiesterase Inhibitors; D014409:Tumor Necrosis Factor-alpha; D010431:Pentoxifylline