ObjectiveTo investigate the effects of remifentanil post-conditioning on apoptosis in renal cells induced by ischemia/reperfusion in rats and the possible mechanism of action.MethodsForty Wistar rats were randomly divided into five groups:sham operation(S group),ischemia-reperfusion(I/Rgroup),remifentanil(1μg/kg/min)postconditioning+I/R(R1 group),remifentanil(2μg/kg/min)postconditioning+I/R(R2group)and remifentanil(4μg/kg/min) postconditioning+I/R(R3group). The bilateral renal pedicels were occluded for 45 minutes using atraumatic vascular clamp then unclamped. In group R1,R2,R3,remifentanil was infused iv at different concentration starting from the moment of ischemia-reperfusion until the rats were killed. Equal volume of normal saline was infused instead of remifentanil in group S and I/R. The animals were killed at 12h of reperfusion respectively. Left kidney were obtained for determination of Bax and Bcl-2 protein expression and apoptosis in kidney cells.ResultsCompared with the control group, the expression of Bcl-2, Bax and apoptosis index was increased in ischemia reperfusion group and remifentanil post-conditioning group( P ?0.05).The expression of Bcl-2 and Bcl-2/Bax ratio was significantly higher , however, the expression of Bax and apoptosis index were significantly lower in remifentanil post-conditioning group than in ischemia reperfusion group( P ?0.05). There was no significant difference between three different remifentanil doses of post-conditioning.ConclusionRemifentanil post-conditioning can reduce nephrocyte apoptosis induced by kidney I/R by changing the balance between Bcl-2 and Bax expression.
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