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机构地区:[1]天津医科大学中西医结合国际学院,天津300070 [2]天津中医药大学第一附属医院,天津300193
出 处:《中国中西医结合肾病杂志》2007年第7期388-390,共3页Chinese Journal of Integrated Traditional and Western Nephrology
摘 要:目的:观察肾疏宁对肾小管间质损害大鼠FN、colm、PAl—lmRNA表达的影响。方法:在系膜增生性肾炎(MsPGN)模型基础上。延长造模时间至12~16周,使其自然发展成肾小管间质损害模型,观察肾疏宁对肾小管间质FN、colm、PAl—lmRNA表达的影响,并设苯那普利为阳性对照组。结果:第12~16周末,造模各组肾小管间质FN、ColⅢ、PAI-1mRNA表达量均明显升高(P〈0.05或P〈0.01),肾疏宁组、苯那普利组均显著低于模型组(P〈0.05或P〈0.01),第12周末,肾疏宁组与苯那普利组比较无统计学差异(P〉0.05),而第16周末,肾疏宁组明显低于苯那普利组(P〈0.01)。结论:肾疏宁能抑制细胞外基质的合成,促进其降解,从而保护肾小管间质损害。Objective:To study the effect of Shenshuning(SSN) on fibronectin (FN),collagen type Ⅲ (ColⅢ) and plasminogen activator inhibitor- 1 (PAl - 1 ) mRNA expression in the animal model of progressive tubulointerstitial injury (TII). Methods:A rat mesangial proliferative glomerulonephritis (MsPGN) model was established, which develops tubulointerstitial lesion at 12-16 weeks. Rats with tubulointerstitial lesions were treated with Shenshuning(SSN), and benazepril was used as positive control. The expression of the FN, Col m and PAl- l mRNA in the tubulointerstitium was examined. Resets: The expression of the FN, COl m and PAl - 1 mRNA in the tubulointerstitium of untreated group significant increased ( P〈 0.05 or P〈 0.01 ) ; SSN and benazepril significantly decreased the expression of the FN, COl m and PAl - 1 mRNA( P 〈 0.05 or P 〈 0.01 ) compared to the untreated controls during 12^th- 16^th weeks. The curative effects of SSN was not significantly different from benazepril at 12^th week( P 〉 0.05 ), but SSN exhibited a distinct advantage over benazepril at 16^th week (P〈 0.01 ). Concision: SSN can inhibit formation of extracellular matrix and promote degradation of extracellular matrix, and protect from tubulointerstitial lesions.
关 键 词:肾小管间质损害 肾疏宁 纤维连接蛋白 Ⅲ型胶原 纤溶酶原激活物抑制剂1
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