Effect of remifentanil on protein kinase C activity during renal ischemia-reperfusion in rats

Abstract

Objective To investigate the effect of remifentanil on protein kinase C (PKC) activity during renal ischemia-reperfusion (I/R) in rats. Methods Seventy-five male Sprague-Dawley rats, weighing 250-300 g, were randomly divided into 5 groups (n=15 each) using a random number table: sham operation group (group S), I/R group, remifentanil group (group R), naloxone group (group N), and naloxone + remifentanil group (group NR). Renal ischemia was induced by clamping the bilateral renal arteries for 45 min using an atraumatic clamp followed by reperfusion.In R and NR groups, remifentanil 1.0 μg·kg-1·min-1was infused via the caudal vein starting from 15 min before ischemia until 30 min of reperfusion.In N and NR groups, naloxone 0.3 mg/kg was injected via the caudal vein at 20 min before ischemia and 35 min of ischemia, respectively.The rats were sacrificed at 24 h of reperfusion and the kidneys were removed for determination of the ultrastructure of the renal tubular epithelial cells (using transmission electron microscope), activity of PKC in renal tissues (by ELISA), and expression of the PKC in renal tissues (by immuno-histochemistry). Results Compared with group S, the activity of PKC in renal tissues was significantly increased in the other four groups, and the expression of the PKC in renal tissues was up-regulated in group R. Compared with group I/R, the activity of PKC in renal tissues was significantlyincreased, the expression of PKC in renal tissues was up-regulated, and the pathological changes were attenuated in group R. Compared with group R, the activity of PKC in renal tissues was significantly decreased, the expression of PKC in renal tissues was down-regulated, and the pathological changes were aggravated in N and NR groups. Conclusion The mechanism by which remifentanil attenuates renal I/R injury may be related to up-regulation of PKC expression and increase in PKC activity through activating opioid receptors in rats. Key words: Piperidines; Reperfusion injury; Kidney; Protein kinase C