Effect of oxycodone pretreatment on cell apoptosis during renal ischemia-reperfusion in rats / 中华麻醉学杂志

ABSTRACT

Objective To evaluate the effect of oxycodone pretreatment on cell apoptosis during renal ischemia-reperfusion (I/R) in rats.Methods Thirty-six healthy male Wistar rats,weighing 180-220 g,aged 6-9 weeks,were divided into 3 groups (n=12 each) using a random number tablesham operation group (group S),renal I/R group (group I/R) and oxycodone pretreatment group (group O).The left renal pedicles were clamped with atraumatic microclips for 45 min followed by reperfusion,and the right kidney was removed immediately after onset of reperfusion to establish the model of renal I/R injury in I/R and O groups.At 10 min before ischemia,oxycodone 0.5 mg/kg was injected via the tail vein in group O,while the equal volume of normal saline was given via the tail vein instead of oxycodone in I/R and S groups.Blood samples were collected by cardiac puncture at 24 h of reperfusion for measurement of serum blood urea nitrogen (BUN) and creatinine (Cr) concentrations.The animals were then sacrificed,and the left renal specimens were obtained for examination of the pathological changes (with a light microscope) and for determination of the expression of Bcl-2,Bax and caspase-3 in renal tissues (by immunohistochemistry).Bcl-2/Bax ratio was calculated.Results Compared with group S,the serum Cr and BUN concentrations were significantly increased,the expression of Bcl-2,Bax and caspase-3 in renal tissues was up-regulated,and the Bcl-2/Bax ratio was decreased in I/R and O groups (P＜0.05).Compared with group I/R,the serum Cr and BUN concentrations were significantly decreased,the expression of Bcl-2 in renal tissues was up-regulated,the expression of Bax and caspase-3 in renal tissues was down-regulated,the Bcl-2/Bax ratio was increased (P＜0.05),and the pathological changes were significantly attenuated in group O.Conclusion The mechanism by which oxycodone pretreatment reduces renal I/R injury may be related to inhibition of cell apoptosis in rats.