Abstract

Objective To evaluate the effect of sufentanil postconditioning on renal ischemia-reperfusion(I/R)injury in rats and the relationship with autophagy. Methods Thirty pathogen-free healthy adult male Wistar rats, aged 6-8 weeks, weighing 180-220 g, were divided into 3 groups(n=10 each)using a random number table: sham operation group(group S), group I/R and sufentanil postconditioning group(group SP). The left renal pedicle was clamped for 45 min with an atraumatic vascular clamp followed by reperfusion, and the right kidney was removed immediately after onset of reperfusion in anesthetized rats to establish the model of renal I/R injury in I/R and SP groups.In group S, the left renal pedicle was only isolated, and the right kidney was removed.Sufentanil 1 μg/kg was injected via the tail vein at 5 min before reperfusion in group SP, while the equal volume of normal saline was given instead in S and I/R groups.At 24 h of reperfusion, blood samples were collected by cardiac puncture for measurement of serum creatinine(Cr)and blood urea nitrogen(BUN)concentrations.The animals were then sacrificed, and the left renal specimens were obtained for examination of pathological changes(with light microscopes)and for determination of the expression of microtubule-associated protein 1 light chain 3(LC3)and Beclin-1 in renal tissues(by immuno-histochemistry). Results Compared with group S, the serum Cr and BUN concentrations were significantly increased, and the expression of LC3 and Beclin-1 in renal tissues was up-regulated(P<0.05), and the pathological changes of kidneys were aggravated in I/R and SP groups.Compared with group I/R, the serum Cr and BUN concentrations were significantly decreased, the expression of LC3 and Beclin-1 in renal tissues was down-regulated(P<0.05), and the pathological changes of kidneys were significantly attenuated in group SP. Conclusion Sufentanil postconditioning can attenuate renal I/R injury, and the mechanism may be related to inhibition of autophagy in rats. Key words: Sufentanil; Ischemic postconditioning; Kidney; Reperfusion injury; Autophagy

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