中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2013年
3期
353-356
,共4页
金小雪%吕艳霞%孟叶%吕会新%熊颖芬%王力利
金小雪%呂豔霞%孟葉%呂會新%熊穎芬%王力利
금소설%려염하%맹협%려회신%웅영분%왕력리
哌啶类%细胞凋亡%再灌注损伤%肾
哌啶類%細胞凋亡%再灌註損傷%腎
고정류%세포조망%재관주손상%신
Piperidines%Apoptosis%Reperfusion injury%Kidney
目的 评价瑞芬太尼对大鼠肾缺血再灌注时细胞凋亡的影响.方法 健康成年雄性SD大鼠75只,体重220~ 250 g,采用随机数字表法,将其分为3组(n=25)∶假手术组(S组)、肾缺血再灌注组(I/R组)和瑞芬太尼组(R组).I/R组和R组采用夹闭双侧肾动脉45 min时恢复灌注法建立肾缺血再灌注损伤模型.R组于缺血前15 min至再灌注30 min经尾静脉输注瑞芬太尼1.0μg· kg-1·min-1,S组和I/R组给予等容量生理盐水.于缺血前15 min(T0)、再灌注3 h(T1)、6 h(T2)、12h(T3)及24 h(T4)时取肾组织标本.采用流式细胞术检测肾细胞凋亡率及Bax、Bcl-2蛋白表达,采用RT-PCR检测Bax和Bcl-2的mRNA表达,计算Bcl-2/Bax蛋白及mRNA表达比值,采用Paller法行肾小管损伤评分.结果 与S组比较,I/R组和R组T1-4时肾小管损伤评分和肾细胞凋亡率升高,Bcl-2/Bax蛋白及mRNA表达比值T12时升高,T3,4时降低(P<0.01);与I/R组比较,R组T1-4时肾小管损伤评分和肾细胞凋亡率降低,Bcl-2/Bax蛋白及mRNA表达比值升高(P<0.05或0.01);与T0时比较,I/R组和R组T1-4时肾小管损伤评分和肾细胞凋亡率升高,Bcl-2/Bax蛋白及mRNA表达比值T1,2时升高,T3,4时降低(P<0.01).结论 瑞芬太尼减轻大鼠肾缺血再灌注损伤的机制与其调节Bcl-2/Bax蛋白表达,抑制肾组织细胞凋亡有关.
目的 評價瑞芬太尼對大鼠腎缺血再灌註時細胞凋亡的影響.方法 健康成年雄性SD大鼠75隻,體重220~ 250 g,採用隨機數字錶法,將其分為3組(n=25)∶假手術組(S組)、腎缺血再灌註組(I/R組)和瑞芬太尼組(R組).I/R組和R組採用夾閉雙側腎動脈45 min時恢複灌註法建立腎缺血再灌註損傷模型.R組于缺血前15 min至再灌註30 min經尾靜脈輸註瑞芬太尼1.0μg· kg-1·min-1,S組和I/R組給予等容量生理鹽水.于缺血前15 min(T0)、再灌註3 h(T1)、6 h(T2)、12h(T3)及24 h(T4)時取腎組織標本.採用流式細胞術檢測腎細胞凋亡率及Bax、Bcl-2蛋白錶達,採用RT-PCR檢測Bax和Bcl-2的mRNA錶達,計算Bcl-2/Bax蛋白及mRNA錶達比值,採用Paller法行腎小管損傷評分.結果 與S組比較,I/R組和R組T1-4時腎小管損傷評分和腎細胞凋亡率升高,Bcl-2/Bax蛋白及mRNA錶達比值T12時升高,T3,4時降低(P<0.01);與I/R組比較,R組T1-4時腎小管損傷評分和腎細胞凋亡率降低,Bcl-2/Bax蛋白及mRNA錶達比值升高(P<0.05或0.01);與T0時比較,I/R組和R組T1-4時腎小管損傷評分和腎細胞凋亡率升高,Bcl-2/Bax蛋白及mRNA錶達比值T1,2時升高,T3,4時降低(P<0.01).結論 瑞芬太尼減輕大鼠腎缺血再灌註損傷的機製與其調節Bcl-2/Bax蛋白錶達,抑製腎組織細胞凋亡有關.
목적 평개서분태니대대서신결혈재관주시세포조망적영향.방법 건강성년웅성SD대서75지,체중220~ 250 g,채용수궤수자표법,장기분위3조(n=25)∶가수술조(S조)、신결혈재관주조(I/R조)화서분태니조(R조).I/R조화R조채용협폐쌍측신동맥45 min시회복관주법건립신결혈재관주손상모형.R조우결혈전15 min지재관주30 min경미정맥수주서분태니1.0μg· kg-1·min-1,S조화I/R조급여등용량생리염수.우결혈전15 min(T0)、재관주3 h(T1)、6 h(T2)、12h(T3)급24 h(T4)시취신조직표본.채용류식세포술검측신세포조망솔급Bax、Bcl-2단백표체,채용RT-PCR검측Bax화Bcl-2적mRNA표체,계산Bcl-2/Bax단백급mRNA표체비치,채용Paller법행신소관손상평분.결과 여S조비교,I/R조화R조T1-4시신소관손상평분화신세포조망솔승고,Bcl-2/Bax단백급mRNA표체비치T12시승고,T3,4시강저(P<0.01);여I/R조비교,R조T1-4시신소관손상평분화신세포조망솔강저,Bcl-2/Bax단백급mRNA표체비치승고(P<0.05혹0.01);여T0시비교,I/R조화R조T1-4시신소관손상평분화신세포조망솔승고,Bcl-2/Bax단백급mRNA표체비치T1,2시승고,T3,4시강저(P<0.01).결론 서분태니감경대서신결혈재관주손상적궤제여기조절Bcl-2/Bax단백표체,억제신조직세포조망유관.
Objective To evaluate the effect of remifentanil on cell apoptosis during renal ischemia-reperfusion (I/R) in rats.Methods Seventy-five male Sprague-Dawley rats,weighing 220-250 g,were randomly divided into 3 groups (n =25 each):sham operation group (group S),I/R group,and remifentanil group (group R).Renal ischemia was induced by occlusion of the bilateral renal arteries for 45 min followed by reperfusion in groups I/R and R.Remifentanil was infused at 1.0 μg· kg-1 · min-1 via the caudal vein starting from 15 min before ischemia until 30 min of reperfusion in group R,while the equal volume of normal saline was given instead of remifentanil in groups S and I/R.At 15 min before ischemia (T0) and 3,6,12,24 h of reperfusion (T1-4),5rats were anesthetized and sacrificed,and renal specimens were obtained to detect the apoptotic rate and expression of Bax and Bcl-2 protein (by flow cytometry) and mRNA (by RT-PCR).The ratios between Bcl-2/Bax protein and mRNA expression were calculated.The pathological changes of renal tubules were scored.Results Compared with group S,the pathological scores and apoptotic rate were significantly increased at T1-4,and ratios between Bcl-2/Bax protein and mRNA expression were increased at T1,2,while decreased at T3,4 in groups R and I/R (P <0.01).Compared with group I/R,the pathological scores and apoptotic rate were significantly decreased at T1-4,while the ratios between Bcl-2/Bax protein and mRNA expression were increased in group R (P < 0.05 or 0.01).Compared with the baseline value at T0,the pathological scores and apoptotic rates were significantly increased at T1 4,and the ratios of Bcl-2/Bax protein and mRNA expression were increased at T1,2,while decreased at T3,4 in groups R and I/R (P < 0.01).Conclusion Regulation of Bcl-2/Bax expression and inhibition of cell apoptosis in renal tissues are involved in the mechanism by which remifentanil reduces renal I/R injury in rats.