Effect of oxycodone pretreatment on renal ischemia-reperfusion injury in rats / 临床麻醉学杂志

ABSTRACT

Objective To evaluate the effects of oxycodone pretreatment on renal ischemiareperfusion(IR) injury in rats.Methods Thirty adult male Sprague-Dawley rats were randomly divided into 3 groups (n=10 each) using a random number tablesham operation group(group S),group IR,and oxycodone pretreatment +IR group (group O).After removing the right kidney in rats,the renal I/R was built by occlusion of the left renal artery and vein for 45 min with a traumatic microclips followed by 2 h reperfusion in I/R and O group.In group S,the right kidney was performed and the left renal artery,vein and ureter were isolated without occluding blood flow.In group O,oxycodone 2 mg/kg were infused intravenously 5 min before onset of ischemia.At 2 h of reperfusion,blood samples were taken from the abdominal aorta to determine the concentrations of serum blood urea nitrogen(BUN)and creatinine(Cr).After blood sampling,the rats were sacrificed,and the left kidney were removed for determination of malondialdehyde(MDA) content (by thiobarbituric acid method) and superoxide dismutase (SOD) activity (using xan-thine oxidase method).The expression levels of B-cell lymphoma-2 (bcl-2),bcl-2 Assaciated X protein(bax) and cycteinyl aspirate-specific protease-3 (Caspase-3) protein were detected by Western blotting,respectively.Results Compared with group S,the serum BUN and Cr concentrations,and the contents of MDA,bax and Caspase-3 in renal tissues were significantly increased,the content of bcl-2 and SOD activity in renal tissues were significantly decreased in the other two groups(P＜0.05).Compared with group IR,the serum BUN and Cr concentrations,and the contents of MDA,bax and Caspase-3 in renal tissues were significantly decreased,the content of bcl-2 and SOD activity in renal tissues were significantly increased in group O (P＜0.05).Conclusion Oxycodone can alleviate renal I/R injury in rats,and the mechanism is related to inhibition of oxidative stress response and cell apoptosis.