Journal
CLINICAL BIOCHEMISTRY
Volume 37, Issue 1, Pages 50-55Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.clinbiochem.2003.10.001
Keywords
ischemia-reperfusion; TNF-alpha; IL-10; anti-IL-12; oxidative stress
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Objectives: 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. Design and 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 I h. Results: Under conditions of IL-12 blockade and IL-10 treatment, I-R-induced tissue TNF-a 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). Conclusion: 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. (C) 2003 The Canadian Society of Clinical Chemists. All rights reserved.
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