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目的:观察糖肾Ⅰ号对早期糖尿病肾病大鼠的干预作用及对周期蛋白(PCNA)表达的影响,分析其可能的作用机制,为临床防治糖尿病肾病提供实验依据。方法:通过单侧肾切除合并注射链脲佐菌素(STZ)建立大鼠早期糖尿病肾病模型,随机分为假手术组(SO)、模型组(M)、糖肾Ⅰ号组(TS)、洛汀新即盐酸贝那普利组(B)、糖洛合组(TS+B)各10只。模型成功后给予不同的干预,连续给药8周,末次给药12小时后,采集尿液、血液标本,酶联免疫吸附法(ELISA)检测尿微量白蛋白(UAlb)和β2-微球蛋白(β2-MG);全自动生化仪检测血清肌酐(Scr)、尿素氮(BUN);摘取右肾,计算肾脏肥大指数(KHI);免疫组织化学法(IHC)检测肾组织蛋白PCNA的表达。结果:与模型组比较,糖肾Ⅰ号组蛋白排泄量明显减少(P<0.01),肾脏肥大指数下降(P<0.05),血清Scr、BUN显著降低(P<0.01),PCNA表达明显下调(P<0.01);各治疗组间比较,以糖洛合组疗效最好。结论:糖肾Ⅰ号具有确切的肾脏保护作用,其作用机制可能部分通过下调PCNA的表达,抑制肾脏肥大,从而发挥肾脏保护作用,与洛汀新合用在改善肾功能方面具有协同作用。
Objective: To observe the effect of Tangshen Ⅰ on the early stage of diabetic nephropathy rats and its effect on the expression of cyclin (PCNA), and to analyze its possible mechanism of action to provide experimental evidence for the prevention and treatment of diabetic nephropathy. Methods: The model of early diabetic nephropathy was established by unilateral nephrectomy combined with streptozotocin (STZ) in rats. The models were randomly divided into three groups: sham operation group (SO), model group (M), Tangshen Ⅰ group (TS) Lotensin, namely benazepril hydrochloride group (B), sugar Luo combination group (TS + B) each 10. After the success of the model, different interventions were given for 8 consecutive weeks. After the last administration for 12 hours, urine and blood samples were collected for detection of urinary albumin (UAlb) and β2-microglobulin by enzyme-linked immunosorbent assay (ELISA) (β2-MG); serum creatinine (Scr) and blood urea nitrogen (BUN) were detected by automatic biochemical analyzer; the right kidney was harvested and the renal hypertrophy index (KHI) was calculated; immunohistochemistry (IHC) . Results: Compared with the model group, the protein excretion of Tangshen Ⅰ group was significantly decreased (P <0.01), the renal hypertrophy index was decreased (P <0.05), the levels of Scr and BUN were significantly decreased (P <0.01) P <0.01); Comparison between the treatment groups, the best effect with the sugar Luohe group. CONCLUSION: Tangshen Ⅰ has definite protective effect on the kidney. The mechanism may be related to the protective effect of kidney partly by down-regulating the expression of PCNA and inhibiting the hypertrophy of kidney, and synergistic with Lotensin in improving renal function.