摘要
目的 探讨瑞芬太尼对大鼠肾缺血再灌注时蛋白激酶C（PKC）活性的影响.方法 清洁级健康成年雄性SD大鼠75只,体重250～ 300 g,采用随机数字表法,将其分为5组（n=15）：假手术组（S组）、缺血再灌注组（I/R组）、瑞芬太尼组（R组）、纳洛酮组（N组）和纳洛酮＋瑞芬太尼组（NR组）.采用夹闭双侧肾动脉45 min恢复灌注的方法制备大鼠肾缺血再灌注损伤模型.R组和NR组于缺血前15 min时尾静脉输注瑞芬太尼1.0 μg·kg^-1 ·min^-1,持续输注90 min;N组和NR组于缺血前20 min时及缺血35 min时尾静脉注射纳洛酮0.3 mg/kg.于再灌注24 h时处死大鼠,取肾组织,透射电镜下观察肾小管上皮细胞超微结构,采用ELISA法确定肾组织PKC活性,采用免疫组化法测定肾组织PKC表达.结果 与S组比较,其余4组肾组织PKC活性升高,R组肾组织PKC表达上调（P＜0.01）;与I/R组比较,R组肾组织PKC活性升高,PKC表达上调（P＜0.01）,病理学损伤减轻;与R组比较,N组和NR组肾组织PKC活性降低,PKC表达下调（P＜0.01）,病理学损伤加重.结论 瑞芬太尼减轻大鼠肾缺血再灌注损伤的机制可能与其通过激活阿片受体,上调PKC表达,升高PKC活性有关.
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.
出处
《中华麻醉学杂志》
CAS
CSCD
北大核心
2015年第1期111-113,共3页
Chinese Journal of Anesthesiology
基金
河北省科学技术研究与发展计划项目（10206133D）
关键词
哌啶类
再灌注损伤
肾
蛋白激酶C
Piperidines
Reperfusion injury
Kidney
Protein kinase C
