CAJ | 학술논문

目的:观察早期应用氨基胍对糖尿病大鼠循环及肾脏血管紧张素Ⅱ(AngⅡ)水平的影响,探讨其对糖尿病肾脏形态、功能的保护作用及潜在AGEs与AngⅡ之间的作用关系.方法:Wistar大鼠随机分组,诱导糖尿病模型后,立即给予糖尿病干预组氨基胍.第12周末检测尿白蛋白排泄率(UAER)、肌酐清除率(Ccr),半定量评分评估肾脏病理改变,放免法、免疫组织化学法分别检测血浆及肾脏AngⅡ水平.结果:与糖尿病对照组相比,氨基胍干预组UAER及肾脏病理改变程度显著减轻(P<0.01),肾脏AngⅡ水平明显减少(P<0.01),血浆Ang Ⅱ水平增加(P<0.01).结论:早期应用氨基胍可能通过阻断AGEs生成从而显著减少肾内AngⅡ水平,抑制局部肾素-血管紧张素系统激活,这可能是氨基胍保护糖尿病大鼠肾脏形态和功能的重要原因之一;氨基胍干预后糖尿病大鼠血浆AngⅡ水平升高可能与局部AngⅡ水平下降后机体的代偿反应有关,具体机制尚需进一步实验证实.
목적:관찰조기응용안기고대당뇨병대서순배급신장혈관긴장소Ⅱ(AngⅡ)수평적영향,탐토기대당뇨병신장형태、공능적보호작용급잠재AGEs여AngⅡ지간적작용관계.방법:Wistar대서수궤분조,유도당뇨병모형후,립즉급여당뇨병간예조안기고.제12주말검측뇨백단백배설솔(UAER)、기항청제솔(Ccr),반정량평분평고신장병리개변,방면법、면역조직화학법분별검측혈장급신장AngⅡ수평.결과:여당뇨병대조조상비,안기고간예조UAER급신장병리개변정도현저감경(P<0.01),신장AngⅡ수평명현감소(P<0.01),혈장Ang Ⅱ수평증가(P<0.01).결론:조기응용안기고가능통과조단AGEs생성종이현저감소신내AngⅡ수평,억제국부신소-혈관긴장소계통격활,저가능시안기고보호당뇨병대서신장형태화공능적중요원인지일;안기고간예후당뇨병대서혈장AngⅡ수평승고가능여국부AngⅡ수평하강후궤체적대상반응유관,구체궤제상수진일보실험증실.
AIM: To investigate the effect of aminoguanidine (AG) on plasma and renal levels of angiogenesis Ⅱ (AngⅡ), and to identify the relationship of AGEs with AngⅡ in STZ-induced diabetic rats. METHODS: Wistar rats were randomly assigned to three groups. Diabetes was induced, rats were then received AG in treatment group. At the end of 12th week, urine albumin excretion rate (UAER) and calculate creatinine clearance (Ccr) were detected. Periodic acid-Schiff reagent was used to evaluate renal pathology. Plasma and renal AngⅡ were analyzed by radioimmunoassay and immunohistochemistry, respectively. RESULTS: AG treatment significantly prevented the increase in UAER (P<0.01), renal pathology (P<0.01), and level of renal AngⅡ (P<0.01). However, plasma concentration of AngⅡ was higher than that in diabetic rats without AG treatment (P<0.01). CONCLUSION: AG down-regulates renal Ang Ⅱ level, probably by reducing the formation of AGEs, which may be one of the renoprotective factors in diabetic nephropathy. More proofs are needed to identify the result that plasma AngⅡ concentration increases in DMA group.