Effect of anti-tumor necrosis factor-alpha monoclonal antibody in alleviating renal ischemia-reperfusion injury.
Shuling Han, Lixin Yu, Junjie Ma, Fang-yin Zeng, Xiaoyou Liu, Xuyong Sun, Haitao Shan, Qian Yuan
Abstract
Shuling Han, Lixin Yu, Junjie Ma, Fang-yin Zeng, Xiaoyou Liu, Xuyong Sun, Haitao Shan, Qian Yuan
Abstract
OBJECTIVE: To investigate the effect of anti-tumor necrosis factor-alpha monoclonal antibody (anti-TNF-alpha mAb) in alleviating renal ischemia-reperfusion injury. METHODS: Fifty normal male Sprague-Dawley rats were randomly divided into 3 groups, namely group A that was subjected to ischemia-reperfusion injury with intravenous administration of anti-TNF-alpha mAb (0.1mg/kg.b.w.) 5 min before reperfusion (treatment group), group B with the same injury followed by saline administration in the same manner (control group), and group C with only anesthetization and leparotomy but not ischemia (sham operation group). Routine assays were performed for testing the levels of blood creatine (Cr), blood urea nitrogen (BUN), plasma TNF-alpha and the cell apoptosis. Ultrastructure of the kidney was also observed. RESULTS: Renal ischemia-reperfusion resulted in significant increase of the levels of Cr, BUN and TNF-alpha in the plasma (P<0.01), but these effects were offset by administration of anti-TNF-alpha mAb (P<0.01). In group B, widespread pathological changes and cell apoptosis were observed in the renal tissue following renal ischemia-reperfusion injury, while similar changes were scarcely visible in group A due to the protective effect of intravenous administration of anti-TNF-alpha mAb 5 min before reperfusion. CONCLUSION: Renal ischemia-reperfusion injury can be alleviated by anti-TNF-alpha mAb treatment.
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OBJECTIVE: To investigate the effect of anti-tumor necrosis factor-alpha monoclonal antibody (anti-TNF-alpha mAb) in alleviating renal ischemia-reperfusion injury. METHODS: Fifty normal male Sprague-Dawley rats were randomly divided into 3 groups, namely group A that was subjected to ischemia-reperfusion injury with intravenous administration of anti-TNF-alpha mAb (0.1mg/kg.b.w.) 5 min before reperfusion (treatment group), group B with the same injury followed by saline administration in the same manner (control group), and group C with only anesthetization and leparotomy but not ischemia (sham operation group). Routine assays were performed for testing the levels of blood creatine (Cr), blood urea nitrogen (BUN), plasma TNF-alpha and the cell apoptosis. Ultrastructure of the kidney was also observed. RESULTS: Renal ischemia-reperfusion resulted in significant increase of the levels of Cr, BUN and TNF-alpha in the plasma (P<0.01), but these effects were offset by administration of anti-TNF-alpha mAb (P<0.01). In group B, widespread pathological changes and cell apoptosis were observed in the renal tissue following renal ischemia-reperfusion injury, while similar changes were scarcely visible in group A due to the protective effect of intravenous administration of anti-TNF-alpha mAb 5 min before reperfusion. CONCLUSION: Renal ischemia-reperfusion injury can be alleviated by anti-TNF-alpha mAb treatment.
Key concepts: Medicine, Renal ischemia, Kidney, Tumor necrosis factor alpha, Reperfusion injury, Ischemia, Blood urea nitrogen, Creatinine