小鼠急性缺血-再灌注肾损伤模型的建立及体会

Model construction of renal acute ischemia-reperfusion injury in mice

目的观察应用小鼠制备急性缺血-再灌注性肾损伤模型的效果。方法应用微型动脉夹夹闭小鼠双侧肾动脉制备急性缺血-再灌注肾损伤模型,其中两组分别于术后24h和48h后处死观察肾功能及肾脏病理变化,另一组观察其病情及存活情况14天。结果各次造模成功率均达85%以上;术后24h及48h实验组血清肌酐(Scr)和血尿素氮(BUN)水平明显升高,与对照组比较差异有统计学意义(P<0.01);实验组肾脏外观出现典型“大白肾”表现,镜下出现典型急性肾小管坏死表现,并有较多炎症细胞浸润,肾小管组织学评分与对照组比较差异有统计学意义(P均<0.01);实验组在观察期间逐渐出现典型急肾衰竭表现,至14天末,死亡率达91.7%,而对照组全部正常存活。结论应用微型动脉夹夹闭小鼠双侧肾动脉可制备稳定急性缺血-再灌注肾损伤模型,而且成功率较高。

Objective To construct the model of renal acute ischemia-reperfusion injury in mice and observe the result of the model. Methods Renal arteries of mice were bilaterally clamped with micro-artery clamps to make model of renal acute ischemia-reperfusion injury. Two groups of animals were sacrificed at 24h and 48h respectively after operation. Renal function and pathology of the mice were examined. The situation of illness and survival in another group of mice were observed for 14 days after operation. Results The successful rate of model was reached to 85% in every model constructing experiment. Levels of serium creatinine （Scr） and blood urea nitrogen （BUN） were remarkably increased in experimental group compared with control group in 24h and 48h after operation （P〈0.01）. In the experimental group, an atypical appearance of ＂large white kedney＂ was seen by grossly and typical acute tubular necrosis with severe inflammatory cells infiltration were found in interstitial area under microscope. Histology score for tubular damage in experimental group was much higher than that of control group （P〈0.01）. Symptoms of acute renal failure were gradually appeared in model animals during observed period, and mortality was reached to 91.7% by the end 14days after operation, While control group was survival normally in all animals. Conclusion Stable model of renal acute ischemia-reperfusion injury of mice can be prepared by applying microartery clamp to incarcerate bilateral mice＇s renal arteries. And it＇s successful rate is very high.