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目的观察尿毒清对阿霉素(ADR)肾病大鼠肾脏转化生长因子-β1(TGF-β1)、金属蛋白酶1组织抑制剂(TIMP-1)、纤溶酶原激活物抑制物1(PAI-1)和骨调素(OPN)mRNA表达的影响,探讨尿毒清治疗慢性肾脏疾病的机制。方法成年雄性SD大鼠24只,采用单侧肾切除加重复尾静脉注射ADR的方法制作ADR肾病模型,随机分为正常组(N组)、模型组(M组)、尿毒清组(Ni组)、贝那普利组(B组)4组,每组6只。用药第4、8周后观察各组大鼠24h尿蛋白定量、血脂、血浆总蛋白(TP)、血浆白蛋白(ALB)、尿素氮(BUN)、肌酐(Scr)的水平,实时荧光定量PCR测定第8周肾组织中TGF-β1、TIMP-1、PAI-1及OPN mRNA的表达。结果尿毒清和贝那普利均能减少ADR肾病大鼠尿蛋白,降低BUN、Scr,升高血浆蛋白,纠正脂代谢紊乱,减少TGF-β1、TIMP-1、PAI-1及OPNmRNA的表达,与M组相比有显著差异(P<0.01);而Ni组PAI-1 mRNA水平较B组显著降低(P<0.01)。结论尿毒清可下调ADR肾病大鼠肾脏组织TGF-β1、TIMP-1、PAI-1及OPN mRNA的合成,可能是其治疗慢性肾脏疾病的重要机制之一。
Objective To observe the effect of uremic buprenorphine on renal transforming growth factor-β1 (TGF-β1), tissue inhibitor of metalloproteinase-1 (TIMP-1), and plasminogen activator inhibitor-1 (PAI-) in rats with adriamycin (ADR) nephropathy. 1) The effect of osteopontin (OPN) mRNA expression was explored to explore the mechanism of urinary toxin treatment of chronic kidney disease. Methods Twenty-four adult male Sprague-Dawley rats were used to produce ADR nephropathy model by unilateral nephrectomy plus repeated tail vein ADR. The models were randomly divided into normal group (N group), model group (M group), and uremic clearance group (Ni group). ), Benazepril group (Group B) 4 groups, 6 in each group. After 4 and 8 weeks of treatment, 24-hour urinary protein quantification, plasma lipids, plasma total protein (TP), plasma albumin (ALB), urea nitrogen (BUN), and creatinine (Scr) levels were observed in each group of rats. Real-time fluorescence quantitative PCR was performed. The expression of TGF-β1, TIMP-1, PAI-1 and OPN mRNA in renal tissue was determined at the 8th week. Results Uremic clearing and benazepril can all reduce the urinary protein of rats with ADR nephropathy, reduce BUN, Scr, increase plasma protein, correct dyslipidemia, reduce the expression of TGF-β1, TIMP-1, PAI-1 and OPN mRNA. There was a significant difference between the M group (P<0.01), while the PAI-1 mRNA level of the Ni group was significantly lower than that of the B group (P<0.01). Conclusion Uremic clearing can down-regulate the synthesis of TGF-β1, TIMP-1, PAI-1 and OPN mRNA in renal tissue of rats with ADR nephropathy, which may be one of the important mechanisms in the treatment of chronic kidney disease.