ABSTRACT
The purpose of this study is to investigate the changes in NF-kappaB and proinflammatory cytokines expression following courses of reperfusion after various cycles of ischemic preconditioning in the rat kidney. Thirty five weeks old Sprague Dawley rats were subjected to 3, 6 and 10 cycles of ischemic preconditioning that composed of 5 min ischemia and 5 min reperfusion at the left common iliac artery using rodent vascular clamp. The left kidney obtained after 0, 3, 6, 24 and 72 hours of reperfusion followed by each cycle. The expression patterns of NF-kappaB, TNF-alpha, IL-1beta and ICAM-1 were detected by immunohistochemical staining and Western blotting methods. Apoptosis were detected by TUNEL assay. The results were as follows; In the ischemic preconditioning group, the mortality increased from 24 hours after reperfusion when cyclic episodes of short ischemia and reperfusion were increased. The highest level of NF-kappaB expression in outer medulla of the kidney from 0 hr to 24 hrs of reperfusion is detected after 10 cycles of ischemic preconditioning. The highest level of NF-kappaB expression at 72 hrs of reperfusion is revealed after 3 cycles of ischemic preconditioning. The highest level of TNF-alpha expression in outer medulla of the kidney at 0 hr and 6, 24, 72hrs of reperfusion is shown after 10 cycles of ischemic preconditioning. After 3 hrs of reperfusion, all ischemic preconditioning groups shows similar expression. The highest level of IL-1beta and ICAM-1 expression in outer medulla of the kidney is observed at all of reperfusion times after 10 cycles of ischemic preconditioning. The highest level of apoptosis in rat kidney outer medulla at all of reperfusion times is shown after 10 cycles of ischemic preconditioning. In conclusion, 3 or 6 times of remote ischemic preconditioning in the common iliac artery could reduce the expression of NF-kappaB, TNF-alpha, IL-1beta, and ICAM-1. However, more than 10 times of remote ischemic preconditioning increased ischemia-reperfusion injury, caused by increased expression of NF-kappaB, TNF-alpha, IL-1beta, and ICAM-1.