Summary Interleukin (IL)‐1 is a major contributor to inflammation and apoptosis during ischemia/reperfusion (I/R) injury. Its deleterious effects are primarily mediated by the activation of nuclear factor‐κB (NF‐κB). Receptor‐binding and signaling of IL‐1 can be blocked by the IL‐1 receptor antagonist (IL‐1ra). The aim of our study was to characterize effects and mechanisms of IL‐1ra administration on inflammation, apoptosis, and infiltration in renal I/R injury. Renal ischemia was induced in Lewis rats by clamping of the left renal artery for 45 min. Kidneys were removed for histological and molecular analysis 24 h or 5 days after reperfusion. IL‐1ra ameliorated I/R induced renal injury and inflammation. Furthermore, the number of apoptotic tubular cells was lower in IL‐1ra‐treated animals 24 h after ischemia, which was paralleled by a Bax/Bcl‐2 mRNA ratio towards anti‐apoptotic effects. IL‐1ra reduced the expression of monocyte chemoattractant protein‐1 (MCP‐1) mRNA at 24 h and 5 days and that of intracellular adhesion molecule‐1 (ICAM‐1) expression at 24 h in the ischemic reperfused kidneys. Our results indicate that IL‐1ra treatment ameliorates renal I/R injury and this protective effect might be mediated by reduced induction of NF‐κB mediated MCP‐1, ICAM‐1, and a decreased ratio between Bax and Bcl‐2 mRNA expression.
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