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目的探讨血管紧张素Ⅱ受体拮抗剂 -氯沙坦钾 (Losartan)对糖尿病肾病肾脏的保护作用。方法 :制作糖尿病大鼠模型 ,模型成功后 ,动物分成 2组 ,治疗组给予氯沙坦钾灌胃 ,糖尿病组给予等量生理盐水 ,设正常对照组 ,亦给予等量生理盐水灌胃。分别于实验的第 1,2 ,4周取肾组织进行石蜡包埋和电镜制样 ,石蜡切片HE ,PAS染色 ,光镜观察 ,超薄切片经铅 -铀双染色 ,电镜观察。结果 :糖尿病组大鼠出现血糖升高 ,肾组织切片PAS染色肾小球系膜区弥漫性增宽 ,肾小球囊壁PAS阳性物明显增多。电镜显示肾小球基底膜不规则增厚、足突融合、系膜外基质增多 ,内皮细胞窗孔消失 ,有的肾小球毛细血管闭锁 ;治疗组肾小球的上述变化明显减轻 ,肾功能显著改善。结论 :动物实验证实氯沙坦钾可抑制肾小球细胞外基质的增生 ,改善肾功能 ,具有肾脏保护作用。
Objective To investigate the protective effect of Losartan on diabetic nephropathy and its mechanism by angiotensin Ⅱ receptor antagonist. Methods: After the model was established successfully, the animals were divided into two groups. The treatment group was given losartan potassium intragastrically. The diabetic group was given the same amount of normal saline. The normal control group was also given normal saline. The kidneys were harvested at the 1st, 2nd, 4th week of the experiment for paraffin embedding and electron microscopy respectively. Paraffin sections were stained with HE and PAS, observed with light microscope and ultrathin sections were observed by electron microscope. Results: The hyperglycemia in diabetic rats was increased. The mesangial area of renal glomerular mesangial area with PAS staining was diffusely broadened, and the positive PAS in glomerular wall was significantly increased. Electron microscopy showed irregular glomerular basement membrane thickening, foot process fusion, mesangial matrix increased endothelial cell disappearance of the window, and some glomerular capillary atresia; treatment group glomerular changes were significantly reduced, renal function Significantly improved. Conclusion: Animal experiments confirmed that losartan potassium can inhibit glomerular extracellular matrix proliferation, improve renal function, with renal protective effect.