摘要
目的:观察1,6-二磷酸果糖(FDP)预处理对急性肾缺血-再灌注损伤的保护作用。方法:新西兰大白兔27只,随机均分为假手术组(S组)、缺血再灌注组(Ⅰ组)、1,6-二磷酸果糖预处理组(F组)。采用左肾切除右肾动静脉夹闭60 min再灌注180 min致肾损伤的模型,术前连续4d给予FDP。缺血-再灌注180 min后分别检测血清肌酐(Scr)、尿素氮(BUN)、肾组织丙二醛(MDA)水平及超氧化物岐化酶(SOD)活性,观察肾组织的病理变化及肾小管计分,并对3组进行比较。结果:与S组比较,I组的Scr、BUN、MDA水平明显升高(P<0.05),SOD活性明显降低(P<0.01)。F组的Scr、BUN、MDA水平均较Ⅰ组明显降低(P<0.01或P<0.05),而SOD活性明显增强(P<0.01)。F组肾组织病理变化轻于Ⅰ组。结论:FDP预处理对兔急性肾缺血-再灌注损伤具有保护作用,该保护作用的机制可能与增强SOD活性,清除过多的氧自由基,减少MDA的生成有关。
Objective. To study the protective effect of the fructose 1,6-diphosphate（FDP） preconditioning on acute renal ischemic reperfusion injury（IRI）. Methods： Tweenty-seven rabbits were divided into 3 groups randomly, sham operation group （group S）; false ischemia-reperfusion group （group I） and FDP preeondiontioning group （ group F）. After FDP or normal saline was administered intravenously Qd for 4d, the renal ichemia-repefusion（I-R） model was established by occlusion of right renal artery and vein for 60min and reperfusion for 180min after left nephroectomy. Serum blood urea nitrogen （BUN）, creatinine （Cr） and superoxide dismutase（SOD） and malonaldehyde （MDA） in renal tissue were detected 3h after reperfusion. Renal histopathology lesions were examined. Results： The level of Ser, BUN, MDA increased significantly（P〈0. 05）, while the activity of SOD decreased signifieanfly（P〈 0. 01） in group Ⅰ compare with group S, group F improved the activity of SOD significantly （P〈0. 01 or P〈0. 05） , decreased the level of Ser, BUN, MDA significantly （P〈0. 01）, comparing with group L Conclusion. Fructose 1,6-diphosphate precondiontioning could protect the kidney from renal ischemia reperfusion injury, the mechanism of protective effect might be related to enhance the activity of SOD, remove excess oxygen free radicals and reduce the generation of MDA.
出处
《四川生理科学杂志》
2010年第1期18-20,共3页
Sichuan Journal of Physiological Sciences
基金
川北医学院校级科研基金资助项目(编号:苗圃08基-06)
关键词
1
6-二磷酸果糖
预处理
肾脏
缺血-再灌注损伤
Fructose 1,6-diphosphate
Preeondiontioning
Kidney
Ischemia-reperfusion injury
