Ppar-γ受体激动剂对糖尿病肾病大鼠肾缺血再灌注的影响  

Effects of Ppar-γ agonists pretreatment on Diabetic nephropathy rats with renal ischemia-reperfusion injury

作　　者：连芳[1] 邓福谋[1] 陆志萍 周志东[1] 徐国海[1] 

机构地区：[1]南昌大学第二附属医院麻醉科,南昌330006 [2]江西省萍乡市第四人民医院,萍乡337000

出　　处：《江西医药》2016年第11期1173-1176,共4页Jiangxi Medical Journal

摘　　要：目的评价Ppar-γ受体激动剂对糖尿病肾病大鼠肾缺血再灌注损伤(I/R)的影响。方法健康清洁级成年雄性Wistar大鼠,体重180-240g,采用高脂高糖饲料+5%葡萄糖水喂养后,小剂量链脲佐菌素腹腔多次注射的方法制备2型糖尿病肾病大鼠(DN大鼠)模型。取制模成功的大鼠30只,使用随机数字表法,随机分为3组(n=10):对照组(DN组)、缺血再灌注组(I/R组)、Ppar-γ受体激动剂组(R组)。于I/R模型建立前给药,R组给予Ppar-γ受体激动剂罗格列酮3mg/kg·d灌胃,DN组和I/R组给予等容量生理盐水灌胃,连续10d。给药结束后I/R组和R组采用切除右肾,夹闭左肾动、静脉45min后恢复灌注的方法制备大鼠肾缺血再灌注模型,DN组切除右肾,不夹闭左肾动、静脉。分别于再灌注24h后心脏采血,测定血清肌酐(Cr)和尿素氮(BUN)浓度,处死大鼠取肾,光镜下观察肾组织形态学变化并进行组织学评分,免疫组化法测定NF-κB表达,对样本NF-κB P65阳性细胞表达范围及强度分别进行半定量评估。结果与DN组比较,I/R组和R组血清肌酐(Cr)及尿素氮(BUN)浓度、肾组织学评分及NF-κB表达升高(P<0.05),与I/R组比较,R组血清肌酐(Cr)及尿素氮(BUN)浓度、肾组织学评分及NF-κB表达降低(P<0.05)。结论 Ppar-γ受体激动剂罗格列酮可减轻糖尿病肾病大鼠肾缺血再灌注损伤,其机制可能与抑制NF-κB活性有关。Objective To evaluate the effect of Ppar-γ receptor agonist on renal ischemia reperfusion injury（I/R） in diabetic nephropathy rats. Methods healthy adult male Wistar rats weighing 180-240 g,the high fat diet ＋5% glucose water feeding method with a small dose of streptozotocin injection preparation of rat model of type 2 diabetic nephropathy. 30 successful rats were randomly divided into 3 groups（n=10）：control group（DN group）,ischemia reperfusion group（I/R group）,Ppar-γreceptor agonist group（R group）. Before the establishment of the I/R model,the R group was given Ppar- gamma receptor agonist rosiglitazone D DN,3mg/kg group and I/R group were given equal volume of normal saline,10 d. After administration,the I/R and R groups were used to remove the right kidney,the left kidney was removed,and the vein was recovered after 45 min. The model of renal ischemia and reperfusion was established. The DN group was removed from the right kidney,and the left renal artery and vein were not clamped. Respectively at 24 h reperfusion heart blood serum creatinine（Cr） and urea nitrogen（BUN） concentration,and then the rats were sacrificed,kidney,under the light microscope to observe the morphological changes of renal tissue and histological score,immunohistochemical method,the expression of NF-κB expression determination,the range and intensity were semi quantitative assessment of the sample of NF-κB P65 positive cells. Results compared with DN group,I/R group and R group,serum creatinine（Cr） and urea nitrogen（BUN） concentration and kidney,NF-κB scores and the increased expression of B（P〈0.05）,compared with I/R group,R group,serum creatinine（Cr） and urea nitrogen（BUN） concentration and kidney,scores and the expression of NF-κB decreased expression（P〈0.05）. Conclusion Ppar-γreceptor agonist rosiglitazone can alleviate renal ischemia reperfusion injury in diabetic nephropathy rats,and its mechanism may be related to the inhibition of NF-κB activity.

关 键 词：Ppar-γ受体激动剂 糖尿病肾病 再灌注损伤 核因子-ΚB 

分 类 号：R587.2[医药卫生—内分泌]