title: Experimental obstructive jaundice results in oxidized low-density-lipoprotein accumulation in surgical wound of rats.
abstract: BACKGROUND
  Mounting evidence suggests that impaired wound healing is a well-defined consequence in obstructive jaundice and, as redox-regulated processes are relevant to wound healing, it is not unreasonable to suppose that oxidative stress associated with lipid peroxidation in cholestasis might be a systemic phenomenon probably comprising all tissues and organs, including wounds. The aim of the present investigation was to analyse the lipid peroxidation status of surgical wounds, in terms of oxidized low-density-lipoprotein (oxLDL) accumulation in experimental obstructive jaundice.
  
  
  METHODS
  Sixteen Wistar-Albino rats weighing 200-230 gr were randomly divided into two groups. Group I (n = 8) was designed as the prolonged obstructive jaundice group and was subjected to bile duct ligation. Group II (Sham-control, n = 8) rats underwent laparotomy alone and bile duct was just dissected from the surrounding tissue. Histopathological evaluation, immunohistochemical screening and immunoflourescent staining of the surgical wound was conducted to the bile-duct ligated rats and control group on the 21st postoperative day.
  
  
  RESULTS
  Wound healing was found to be impaired in jaundiced rats histopathologically. When compared with the control group, significant positive oxLDL staining and intracellular accumulation of TNF-alpha, IL-2 and IL-6 was detected in the wound sections of the prolonged obstructive jaundice group.
  
  
  CONCLUSIONS
  Our present data is the first in the literature, indicating significant oxLDL accumulation in surgical wounds of cholestatic rats, which might be one of the results of systemic oxidative stress leading to deficient healing capacity as a consequence of persistent inflammation.
authors.affiliation: Department of Surgery, Zonguldak Karaelmas University, The School of Medicine, Kozlu-Zonguldak, Turkey. gkkaradeniz@yahoo.com
authors.forename: G Karadeniz
authors.initials: GK
authors.lastname: Cakmak
authors.forename: O
authors.initials: O
authors.lastname: Tascilar
authors.forename: I O
authors.initials: IO
authors.lastname: Tekin
authors.forename: B H
authors.initials: BH
authors.lastname: Ucan
authors.forename: A U
authors.initials: AU
authors.lastname: Emre
authors.forename: B D
authors.initials: BD
authors.lastname: Gun
authors.forename: S
authors.initials: S
authors.lastname: Acikgoz
authors.forename: F
authors.initials: F
authors.lastname: Barut
authors.forename: O
authors.initials: O
authors.lastname: Irkorucu
authors.forename: K
authors.initials: K
authors.lastname: Karakaya
authors.forename: H
authors.initials: H
authors.lastname: Balbaloglu
authors.forename: M
authors.initials: M
authors.lastname: Comert
mesh_terms: D000818:Animals; D007150:Immunohistochemistry; D007376:Interleukin-2 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D041781:Jaundice, Obstructive / Q000378:metabolism*; D015227:Lipid Peroxidation / Q000502:physiology; D008077:Lipoproteins, LDL / Q000378:metabolism*; D008297:Male; D018384:Oxidative Stress / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014945:Wound Healing / Q000502:physiology*
chemical_list: D007376:Interleukin-2; D015850:Interleukin-6; D008077:Lipoproteins, LDL; D014409:Tumor Necrosis Factor-alpha