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目的探讨大鼠阿霉素肾病(ADR)肾组织转化生长因子β1(TGF-β1)、血小板源性生长因子-BB(PDGF-BB)、结缔组织生长因子(CTGF)的表达与肾间质纤维化的关系及莫索尼定对其影响。方法2004年8月至2004年11月选取哈尔滨医科大学动物实验中心的60只雄性健康Wistar大鼠随机分为健康对照组、模型组及莫索尼定(MOX)治疗组,两次阿霉素尾静脉注射建立模型,治疗组给予MOX1·5mg/(kg·d);分别于4、8、12周末留取标本,测定24h蛋白尿、血生化、肾组织分别进行透射电镜及HE、Mas-son染色,应用免疫组织化学方法检测肾组织中的TGF-β1、PDGF-BB、CTGF蛋白的表达。结果血压、生化指标在治疗组和模型组差异无显著性,模型组24h尿蛋白排泄率高于对照组,差异有显著性(P<0·05),治疗组24h蛋白尿明显低于模型组,差异有显著性(P<0·05),与对照组比较模型组肾小管、肾间质呈明显病理改变,差异有显著性(P<0·05),治疗组损伤较模型组减轻,差异有显著性(P<0·05)。PDGF-BB蛋白表达于第4周,TGF-β1、CTGF蛋白表达第8周开始明显上调,与肾间质纤维化程度呈正相关,莫索尼定治疗组上述生长因子表达下调,差异均有显著性(P<0·05)。结论在大鼠阿霉素肾病肾组织中,肾间质纤维化与TGF-β1、PDGF-BB、CTGF蛋白高表达有关,莫索尼定通过下调促纤维化因子的表达,从而发挥其延缓肾纤维化及肾小球硬化作用。
Objective To investigate the expression of transforming growth factor-β1 (TGF-β1), platelet-derived growth factor-BB (PDGF-BB) and connective tissue growth factor (CTGF) in rat adriamycin nephropathy (ADR) The relationship between Moxonidine and its influence. Methods From August 2004 to November 2004, 60 male healthy Wistar rats from Harbin Medical University Animal Experimental Center were randomly divided into healthy control group, model group and moxonidine (MOX) group, two doxorubicin The model was established by intravenous injection. The treatment group was given MOX 1.5 mg / (kg · d). The specimens were collected at the end of 4, 8 and 12 weeks respectively. Proteinuria, blood biochemistry and renal tissue were determined by transmission electron microscopy, HE and Mas-son The expression of TGF-β1, PDGF-BB and CTGF protein in renal tissues was detected by immunohistochemistry. Results There was no significant difference in blood pressure and biochemical indexes between the treatment group and the model group. The urinary protein excretion rate in the model group was higher than that in the control group (P <0.05), and the proteinuria 24h in the treatment group was significantly lower than that in the model group , The difference was significant (P <0.05). Compared with the control group, the pathological changes of renal tubule and renal interstitium in the model group showed significant difference (P <0.05), the treatment group lessened the injury compared with the model group, The difference was significant (P <0.05). At the 4th week, the expression of PDGF-BB protein was up-regulated from the 8th week, and positively correlated with the degree of renal interstitial fibrosis. The expression of PDGF-BB was down-regulated in the Moxonidine group (P <0.05). Conclusion In rat adriamycin-induced nephropathy, renal interstitial fibrosis is associated with high expression of TGF-β1, PDGF-BB and CTGF protein. Moxonidine may play a role in retarding renal fibrosis by decreasing the expression of pro-fibrosis factor And glomerular sclerosis.