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首页> 外文期刊>Life sciences >Losartan ameliorates progression of glomerular structural changes in diabetic KKAy mice.
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Losartan ameliorates progression of glomerular structural changes in diabetic KKAy mice.

机译：氯沙坦改善了糖尿病KKAy小鼠肾小球结构变化的进程。

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Pathological changes in glomerular structure are typically associated with the progression of diabetic nephropathy. The involvement of angiotensin II (AII) in pathogenesis of diabetic nephropathy has been extensively studied and the therapeutic advantages associated with blockade of renin-angiotensin system (RAS), primarily with angiotensin converting enzyme (ACE) inhibitors, has been well-documented. We studied the effect of RAS blockade with an AII receptor antagonist (losartan) vs. an ACE inhibitor (enalapril) on glomerular lesions in KKAy mice, a model of type 2 diabetes mellitus. Losartan was administered at 3 and 10 mg/kg/day and enalapril at 3 mg/kg/day for 14 weeks in the drinking water. The doses of losartan at 10 mg/kg/day was expected to be equivalent to 3 mg/kg/day of enalapril when considering clinical doses for lowering blood pressure. The dose of 3 mg/kg/day of losartan was selected to compare the efficacy at equivalent dose of enalapril. Histologic observation demonstrated suppression of glomerular mesangial expansion and glomerulosclerosis with exudative lesion in the 10 mg/kg/day losartan group when compared to the untreated diabetic controls. A lesser degree of glomerulosclerosis was also observed with losartan and enalapril treatment at 3 mg/kg/day. Ultrastructural examination of renal glomeruli from the high dose losartan group revealed a decreased degree of effacement and/or irregular arrangement of glomerular podocytic foot process. The beneficial effect of RAS inhibition with the AII receptor antagonist losartan on diabetic glomerular lesions was clearly demonstrated in this study. These findings, therefore, provide mechanistic explanation for the clinical utility of losartan for use in the treatment of diabetic nephropathy in man.
机译：肾小球结构的病理变化通常与糖尿病性肾病的进展有关。血管紧张素II（AII）参与糖尿病性肾病的发病机理已得到广泛研究，并且与肾素-血管紧张素系统（RAS）阻断相关的治疗优势（主要是血管紧张素转化酶（ACE）抑制剂）已得到充分证明。我们研究了用AII受体拮抗剂（氯沙坦）与ACE抑制剂（依那普利）进行的RAS阻断对2型糖尿病模型KKAy小鼠肾小球病变的影响。在饮用水中以3和10 mg / kg /天的剂量施用氯沙坦，以3 mg / kg /天的剂量施用依那普利14周。当考虑降低血压的临床剂量时，氯沙坦的10 mg / kg /天的剂量预期相当于3 mg / kg /天的依那普利。选择3 mg / kg /天的氯沙坦剂量以比较等效剂量的依那普利的疗效。组织学观察表明，与未经治疗的糖尿病对照组相比，10 mg / kg /天的氯沙坦组抑制了肾小球系膜扩张和肾小球硬化伴渗出性病变。氯沙坦和依那普利以3 mg / kg /天的剂量治疗时，肾小球硬化程度也较低。高剂量氯沙坦组肾小球的超微结构检查显示肾小球足底突突的脱落程度降低和/或排列不规则。这项研究清楚地证明了用AII受体拮抗剂洛沙坦抑制RAS对糖尿病肾小球病变的有益作用。因此，这些发现为氯沙坦用于治疗人类糖尿病性肾病的临床实用性提供了机械解释。

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