title: Study of the Role of Transforming Growth Factor β-1 in Organ Damage Protection in Porcine Model of Brain Death.
abstract: BACKGROUND
  From the medical and ethical points of view, donation after brain death is a more acceptable organ source than that from a living donor because it has the advantage of providing multiple organs from a single donor source. Hence, it has become a more promising field of research which focuses on the protection of organs at brain death Here we investigated the role of transforming growth factor (TGF)-β1 in a porcine model of brain death.
  
  
  METHODS
  A porcine model of brain death was established by increasing the intracranial pressure (ICP) after which TGF-β1 was monitored by immunofluorescence at the following time points: before ICP was performed (t1), at brain death (t2), and at 3 (t3), 6 (t4), 9 (t5), and 18 (t6) hours after brain death. The data were analyzed using the fixed effect regression method and the correlation between the results was determined by Pearson analysis.
  
  
  RESULTS
  Our results showed that there was a significant increase in the levels of TGF-β1 (P < .05), urea (P < .01), creatinine (P < .01), and aspartate aminotransferase (AST; P < .01) during the 18-hour brain death process. There were negative correlations between TGF-β1 and urea, creatinine, alanine aminotransferase, AST, and total bilirubin. The negative correlations between TGF-β1 and creatinine and AST achieved statistical significance (P < .05).
  
  
  CONCLUSIONS
  These findings taken together confirm that significant damages are caused to the myocardial fiber cell and kidney glomerulus during brain death process, and that TGF-β1 is associated with the protection of these organs.
authors.affiliation: Department of Clinical Laboratory, The First Central Hospital of Tianjin, Tianjin, China.
authors.forename: L
authors.initials: L
authors.lastname: Chen
authors.affiliation: Department of Neurosurgery, The First Central Hospital of Tianjin, Tianjin, China.
authors.forename: X
authors.initials: X
authors.lastname: Feng
authors.affiliation: Key Laboratory for Critical Care Medicine of the Ministry of Health, Tianjin, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Key Laboratory for Critical Care Medicine of the Ministry of Health, Tianjin, China.
authors.forename: X
authors.initials: X
authors.lastname: Xu
authors.affiliation: Department of Neurosurgery, The First Central Hospital of Tianjin, Tianjin, China.
authors.forename: C
authors.initials: C
authors.lastname: Wan
authors.affiliation: Department of Transplantation Surgery, The First Central Hospital of Tianjin, Tianjin, China.
authors.forename: J
authors.initials: J
authors.lastname: Wang
authors.affiliation: Department of Clinical Laboratory, The First Central Hospital of Tianjin, Tianjin, China. Electronic address: 2356677342@qq.com.
authors.forename: H
authors.initials: H
authors.lastname: Mu
mesh_terms: D000818:Animals; D001219:Aspartate Aminotransferases / Q000378:metabolism; D001663:Bilirubin / Q000378:metabolism; D001926:Brain Death / Q000378:metabolism*; D003404:Creatinine / Q000378:metabolism; D007427:Intracranial Pressure; D007678:Kidney Glomerulus / Q000378:metabolism; D023421:Models, Animal; D009206:Myocardium / Q000378:metabolism; D013552:Swine; D013997:Time Factors; D020858:Tissue and Organ Harvesting; D053773:Transforming Growth Factor beta1 / Q000378:metabolism*; D014508:Urea / Q000378:metabolism
chemical_list: D053773:Transforming Growth Factor beta1; D014508:Urea; D003404:Creatinine; D001219:Aspartate Aminotransferases; D001663:Bilirubin