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 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). 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.
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 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). 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.