To investigate the effects of ischemic preconditioning on renal injury in ischemia-reperfused kidneys.

A total of 60 rats undergoing right nephrectomy were randomized to the following groups: group 1, sham-operated control; group 2, 45 minutes ischemia alone; group 3, 5 minutes of ischemia followed by 5 minutes of reperfusion before 45 minutes of ischemia. The left kidneys of 5 rats were removed immediately and 6, 12, and 24 hours after the surgical procedure. The concentrations of nitric oxide (NO) metabolites were measured using the Griess method, and the expression levels of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) and clusterin were determined by real-time reverse transcriptase-polymerase chain reaction. The degree of renal injury was evaluated using the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end assay.

No significant changes were found in the serum or renal concentrations of the NO metabolites or the expression levels of renal LOX-1 and clusterin in group 1. The serum and renal concentrations of the NO metabolites in group 3 were significantly greater than those in group 2 at 24 and 12 hours after reperfusion, respectively. The LOX-1 expression in group 3 was significantly downregulated compared with that in group 2 at 6 and 12 hours after reperfusion, and the clusterin expression level in group 3 was significantly greater than that in group 2 at 6 and 12 hours after reperfusion. The degree of renal injury in group 2 was significantly more severe than in groups 1 and 3.

Pretreatment of ischemic preconditioning resulted in the induction of protective effects on ischemia/reperfusion-induced injury through the inhibition of apoptosis, in which enhanced production of NO and downregulation of LOX-1 induced by ischemic preconditioning might be involved.