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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 effect of advanced glycation end products (AGEs) on the expression of angiotensin converting enzyme 2 (ACE2) in the kidney of diabetic rats. Methods After induction of diabetic model, aminoguanidine was given to diabetic rats in intervention group immediately. Urine albumin excretion rate (UAER), renal extramembranous matrix hyperplasia (MME) were measured at the end of the 12th week. ACE2 and ACE protein expressions were measured in the kidney. ACE2 / ACE ratio was calculated and renal ACE2 mRNA levels were measured. Results Compared with diabetic control group, aminoguanidine intervention group decreased UAER and MME (P <0.05), renal ACE2 expression and ACE2 / ACE ratio increased (P <0.05). Conclusion AGEs can down-regulate the expression of ACE2 in the kidney of diabetic rats and decrease the ACE2 / ACE ratio, which may be one of the important causes of diabetic nephropathy.