糖基化终产物对糖尿病大鼠肾脏血管紧张素转换酶2表达的调节  

Effects Of advanced glycation end-products on renal ACE 2 expression in streptozotocin-induced diabetic rats

作　　者：刘帅[1] 沈洁[1] 唐杰龙[1] 范艳飞[1] 谢翠华[1] 薛耀明[1] Ryoji Nagai 

机构地区：[1]南方医科大学附属南方医院内分泌代谢科,广州510515

出　　处：《中国糖尿病杂志》2010年第7期504-506,共3页Chinese Journal of Diabetes

基　　金：广东省科技计划项目(2007B010600010)

摘　　要：目的观察糖基化终产物(AGEs)对糖尿病大鼠肾脏血管紧张素转换酶2(ACE2)表达的调节和意义。方法诱导糖尿病模型后,立即给予干预组糖尿病大鼠氨基胍。第12周末检测尿白蛋白排泄率(UAER)、肾脏系膜外基质增生(MME),测定肾内ACE2、ACE蛋白表达,计算ACE2/ACE比值,并检测肾脏ACE2mRNA水平。结果与糖尿病对照组相比,氨基胍干预组UAER及MME降低(P<0.05),肾脏ACE2表达及ACE2/ACE比值增加(P<0.05)。结论 AGEs可下调糖尿病大鼠肾脏ACE2表达,减少ACE2/ACE比值,可能是导致糖尿病肾病的重要原因之一。Objective To investigate the effects of advanced glycation end-products （AGEs） on renal ACE 2 in diabetic rats. Methods Diabetes was induced, diabetic rats received aminoguanidine （AG） in treatment group. At the end of 12th week, urine albumin excretion rate （UAER） and mesangial matrix expansion （MME） were detected. ACE 2 expression was analyzed by immunohistochemistry and RT-PCR. The ratio of ACE2/ACE was evaluated. Results AG treatment significantly prevented the increasing of UAER and MME （P〈0.05）, and increased the renal expression of ACE2 and the ratio of ACE2/ACE as compared with that in diabetic group without AG （P〈0.05）. Conclusions This is the first data to demonstrate AGEs can down-regulate ACE2 expression and decrease the ratio of ACE2/ACE, which may be one of key pathogenesis of diabetic nephropathy.

关 键 词：糖基化终产物 血管紧张素转换酶2 糖尿病肾病 

分 类 号：R587.1[医药卫生—内分泌]