论文部分内容阅读
目的:观察Smad在糖尿病大鼠肾脏中的表达及保元Ⅱ号对其表达的影响。方法:用链脲佐菌素腹腔注射制备糖尿病大鼠模型,随机分为空白对照组(N),模型组(DN),保元Ⅱ号治疗组(Z)和贝那普利治疗组(B),并用相应的药物干预,给药8周后处死大鼠,检测各组血浆白蛋白、血糖、尿蛋白定量、尿β2微球蛋白含量,并且用RT-PCR检测TGF-β1和Smad2,Smad3,Smad7在肾组织的表达水平。结果:与DN组相比,DN-Z组血浆白蛋白明显上升(P<0.01),血糖和尿蛋白定量、尿β2微球蛋白水平均有下降(P<0.01);TGF-β1、Smad2、Smad3的mRNA在模型大鼠肾组织中表达明显下调,Smad7的mRNA明显下调。干预效果与贝那普利相近。结论:保元Ⅱ号对糖尿病大鼠肾脏有保护作用,其机制可能与调节肾脏中TGF-β1和Smad2,Smad3,Smad7表达水平有关。
Objective: To observe the expression of Smad in the kidney of diabetic rats and the effect of Baoyuan II on its expression. METHODS: Diabetic rat models were prepared by intraperitoneal injection of streptozotocin and randomly divided into control group (N), model group (DN), Baoyuan II treatment group (Z) and benazepril treatment group (B ), and with the corresponding drug intervention, after 8 weeks of administration, the rats were sacrificed and the plasma albumin, blood glucose, urinary protein, and urinary β2 microglobulin levels were measured in each group, and TGF-β1 and Smad2, Smad3 were detected by RT-PCR. The expression level of Smad7 in kidney tissue. Results: Compared with DN group, serum albumin in DN-Z group increased significantly (P<0.01), blood glucose and urinary protein quantification, urine β2 microglobulin level decreased (P<0.01); TGF-β1, Smad2, The mRNA expression of Smad3 was significantly down-regulated in the kidney of model rats, and mRNA of Smad7 was significantly down-regulated. The effect of intervention is similar to that of benazepril. Conclusion: Baoyuan II has a protective effect on the kidney of diabetic rats, and its mechanism may be related to the regulation of the expression of TGF-β1 and Smad2, Smad3 and Smad7 in the kidney.