title: Effect of propofol on mucous permeability and inflammatory mediators expression in the intestine following traumatic brain injury in rats.
abstract: OBJECTIVE
  To explore whether propofol could in vivo, suppress intestinal permeability and proinflammatory cytokines in the intestine after traumatic brain injury (TBI).
  
  
  METHODS
  The rats were randomly divided into four groups including control group with right parietal bone window alone and no brain injury, TBI group, TBI+propofol (5mg/kg/h), and propofol alone group. All animals were killed 72h later. Plasma endotoxin was assayed by the chromogenic limulus amebocyte lysate test. Intestinal permeability was quantified using the lactulose/mannitol (L/M) test. TNF-alpha and IL-6 in the intestine were measured using commercially available enzyme-linked immunoassay Kits. Nuclear factor kappa B (NF-kappaB) was analyzed by Electrophoretic mobility shift assay (EMSA).
  
  
  RESULTS
  No rats died before sacrifice. Plasma endotoxin, L/M ratio, intestinal level of NF-kappaB, TNF-alpha, and IL-6 remained at baseline level in controlled animals. TBI promoted a significant increment in plasma endotoxin, L/M ratio, intestinal level of NF-kappaB, TNF-alpha, and IL-6. Propofol inhibited those parameters at the dose of 5mg/kg/h.
  
  
  CONCLUSIONS
  Propofol has the protective effect on the intestine following traumatic brain injury in rats.
authors.affiliation: Department of Anesthesiology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing 210029, PR China.
authors.forename: Jie
authors.initials: J
authors.lastname: Sun
authors.forename: Lin
authors.initials: L
authors.lastname: Wang
authors.forename: Jinchun
authors.initials: J
authors.lastname: Shen
authors.forename: Zhongyun
authors.initials: Z
authors.lastname: Wang
authors.forename: Yanning
authors.initials: Y
authors.lastname: Qian
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D004305:Dose-Response Relationship, Drug; D004731:Endotoxins / Q000097:blood*; D005786:Gene Expression Regulation / Q000187:drug effects; D006993:Hypnotics and Sedatives / Q000494:pharmacology*; D018836:Inflammation Mediators / Q000378:metabolism*; D015850:Interleukin-6 / Q000096:biosynthesis; D007413:Intestinal Mucosa / Q000378:metabolism* / Q000473:pathology; D008297:Male; D016328:NF-kappa B / Q000096:biosynthesis; D010539:Permeability / Q000187:drug effects; D015742:Propofol / Q000494:pharmacology*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D004731:Endotoxins; D006993:Hypnotics and Sedatives; D018836:Inflammation Mediators; D015850:Interleukin-6; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D015742:Propofol