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目的:观察药物对阿霉素肾病大鼠模型nephrin的影响,探讨肾特灵加泼尼松治疗肾病综合征的作用机制。方法:采用阿霉素建立大鼠肾病模型,并随机分为模型组、泼尼松组、肾特灵加泼尼松组(综合组)各10只,另设正常对照组(10只);检测用药后24h尿蛋白定量、血清白蛋白(Alb)、胆固醇(Chol)、血肌酐(Scr)及尿素氮(BUN);采用反转录-聚合酶链反应(RT—PCR)方法检测nephrin。结果:给药后。在同一时间点泼尼松组、综合组24h尿蛋白量均明显低于模型组(P<0.01);综合组尿蛋白定量、Alb、Chol、Scr、BUN均较泼尼松组改善,差异有显著性或非常显著性意义(P<0.05,P<0.01);与对照组比较,模型组nephrin下调70%、泼尼松组nephrin下调38%、肾特灵加泼尼松组nephrin下调22%。结论:nephrin的表达减少是大量蛋白尿的主要原因;肾特灵加泼尼松治疗肾病综合征的作用机制之一是提高肾小球细胞nephrin的表达,其治疗作用优于单纯使用泼尼松。
OBJECTIVE: To observe the effect of drugs on nephrin in adriamycin-induced nephropathy rat model and to explore the mechanism of nephrotoxic and prednisone treatment of nephrotic syndrome. Methods: A rat model of nephropathy was established by adriamycin and randomly divided into model group, prednisone group, tramadol plus prednisone group (n = 10) and normal control group (n = 10). Urine protein, serum albumin (Alb), cholesterol (Chol), serum creatinine (Scr) and blood urea nitrogen (BUN) were measured 24h after treatment. Nephrin was detected by reverse transcription-polymerase chain reaction (RT- Results: After administration. In the prednisone group at the same time point, the 24-hour urinary protein levels in the integrated group were significantly lower than those in the model group (P <0.01). The levels of Alb, Chol, Scr and BUN in the comprehensive group were better than those in the prednisone group (P <0.05, P <0.01). Compared with the control group, nephrin decreased by 70% in the model group, nephrin decreased by 38% in the prednisone group and decreased by 22% in the combination of Shen Trang plus prednisone group . CONCLUSIONS: The decrease of nephrin expression is the main reason of massive proteinuria. One of the mechanisms of nephrotic syndrome induced by nesiritide and prednisone is to improve the expression of nephrin in glomerular mesangial cells. The therapeutic effect is better than that of prednisone alone .