کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3866123 | 1598963 | 2010 | 8 صفحه PDF | دانلود رایگان |
PurposeThere is increasing evidence that ischemic postconditioning may noticeably attenuate renal ischemic-reperfusion injury, although the specific mechanisms are not fully clear. We examined the role of the complement system, especially membrane bound complement regulatory proteins, in postconditioning after renal ischemic-reperfusion injury in a right nephrectomy rat model.Materials and MethodsAfter right nephrectomy the left renal pedicles were occluded for 60 minutes, followed by 24-hour reperfusion. Postconditioning was induced by 6 cycles of 10-second ischemia and 10-second reperfusion before reperfusion. After 24-hour reperfusion without a control blood samples were obtained via the vena cava. Renal samples were also obtained. DAF, CD46, CD59, C3aR and C5aR mRNA and protein expression was examined by reverse transcriptase-polymerase chain reaction, Western blot and immunohistochemistry. C3/C9 deposition in tissue was detected by immunofluorescence. Renal function, histology and cellular apoptosis were also observed.ResultsIn renal tissue postconditioning prevents DAF down-regulation, which is induced by ischemic-reperfusion injury. It results in the decreased renal necrosis caused by ischemic-reperfusion injury mediated complement activation. However, in all experimental groups renal CD46/CD59 expression was not altered. Increased DAF expression due to postconditioning may decrease C5aR expression in renal tissues compared with ischemic-reperfusion injury, which can decrease apoptosis. C3aR expression did not differ among the experimental groups.ConclusionsThese findings provide new evidence that postconditioning protects kidneys from ischemic-reperfusion injury, at least in part, by preventing DAF down-regulation.
Journal: The Journal of Urology - Volume 183, Issue 6, June 2010, Pages 2424–2431