title: Which is more effective in the prevention of renal ischemia-reperfusion-induced oxidative injury in the early period in mice: interleukin (IL)-10 or anti-IL-12?
abstract: OBJECTIVE
  Ischemia-reperfusion (I-R) injury induces production of reactive oxygen species (ROS) and some inflammatory mediators like tumor necrosis factor (TNF). We compared the effects of IL-10 and anti IL-12 antibody (Ab) on TNF-alpha production and oxidative stress markers. We also searched for which one, anti IL-12 or IL-10, is superior in the prevention of I-R induced oxidative stress.
  
  
  METHODS
  The animals were divided into four groups: control (n = 5), I-R (n = 5), I-R + IL-10 (n = 5), I-R + anti IL-12 Ab (n = 5). Mice were subjected to renal ischemia by clamping the left pedicle for 45 min, and were then reperfused for 1 h.
  
  
  RESULTS
  Under conditions of IL-12 blockade and IL-10 treatment, I-R-induced tissue TNF-alpha levels were significantly reduced (P < 0.01). IL-10 treatment decreased I-R-induced thiobarbituric acid reactive substances (TBARS) and protein carbonyl content levels (P < 0.05). After IL-10 treatment, decrease in tissue reduced glutathione (GSH) levels were prevented. Renal superoxide dismutase (SOD) and catalase (CAT) activities were observed to be decreased after I-R. IL-10 treatment increased both SOD and CAT activities over control values (P < 0.05).
  
  
  CONCLUSIONS
  These data indicated that IL-10 treatment may be more effective than anti-IL-12 treatment in the prevention of renal I-R-induced oxidative injury in the early period.
authors.affiliation: Department of Biochemistry, School of Medicine, Afyon Kocatepe University, Afyon, Turkey. tkoken@aku.edu.tr
authors.forename: Tülay
authors.initials: T
authors.lastname: Köken
authors.forename: Mustafa
authors.initials: M
authors.lastname: Serteser
authors.forename: Ahmet
authors.initials: A
authors.lastname: Kahraman
authors.forename: Gökhan
authors.initials: G
authors.lastname: Akbulut
authors.forename: Osman Nuri
authors.initials: ON
authors.lastname: Dilek
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D005978:Glutathione / Q000096:biosynthesis; D016753:Interleukin-10 / Q000627:therapeutic use*; D018664:Interleukin-12 / Q000627:therapeutic use*; D007674:Kidney Diseases / Q000503:physiopathology / Q000517:prevention & control*; D015227:Lipid Peroxidation; D008297:Male; D051379:Mice; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000473:pathology / Q000517:prevention & control*; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D018664:Interleukin-12; D002374:Catalase; D013482:Superoxide Dismutase; D005978:Glutathione