苯那普利防治肾小球硬化的实验研究  

A STUDY ON THE MECHANISM OF BENAZIPRIL IN PREVENTING THE PROGERSSION OF GLOMERULOSCLEROSIS

作　　者：王文新[1] 陈香美[1] 叶一舟[1] 师锁柱[1] 于志恒[1] 

机构地区：[1]解放军总医院,北京100853

出　　处：《解放军医学杂志》2001年第6期432-434,共3页Medical Journal of Chinese People's Liberation Army

基　　金：全军"九五"重点课题资助! (编号 95 2 0 5 6 )

摘　　要：用 5 /6肾切除法造模大鼠肾小球硬化并给予苯那普利治疗 2 0周 ,观察苯那普利对大鼠残肾组织Ⅳ型胶原和基质金属蛋白酶 9(MMP 9) /组织金属蛋白酶抑制物 1(TIMP 1)基因表达的影响 ,旨在揭示其减轻肾小球硬化的机制。结果苯那普利能显著减轻大鼠肾组织的病理改变程度 ,并且显著减少残肾组织中Ⅳ型胶原、MMP 9的沉积以及下调Ⅳ型胶原、MMP 9/TIMP 1的基因表达。苯那普利可能通过调节MMP 9/TIMP 1的基因表达 ,减轻肾小球重塑过程中细胞外基质的异常代谢和聚积 。nephrectomy in Wistar rats were used to replicate the animal model of focal and segmental glomerular sclerosis.Then a group of 5/6 nephrectomized rats were given Benzaipril for 20 weeks , in order to evaluate the effects of Benazipril on degradation of extracellular matrix. The results showed that Benzipril not only reduced renal pathological changes, but also significantly decreased the type Ⅳ collagen and MMP 9 deposition and down regulated the mRNA expressions of MMP 9 and TIMP 1 in the remnant kidneys of the 5/6 nephrectomized rats. It suggested that Benzipril might ameliorate glomerulosclerosis through the mechanism of modulating extracellular matrix degradation in the remnant kidney tissue.

关 键 词：苯那普利 肾小球硬化症 MMP-9基因 TIMP-1基因 基因表达 

分 类 号：R692.6[医药卫生—泌尿科学]