摘要
目的研究贝那普利联合胰激肽原酶对实验性肾间质纤维化模型大鼠肾脏是否具有保护作用及其可能的机制。方法 60只SD大鼠分为假手术组(A组)、模型组(B组)、贝那普利治疗组(C组)和贝那普利联合胰激肽原酶治疗组(D组),观察肾组织病理变化,血管紧张素Ⅱ(AngⅡ)和血小板源性生长因子(PDGF-B)的表达情况。结果 D组治疗14d后较其余3组,可减少AngⅡ的含量(P<0.05),下调PDGF-B的表达(P<0.05),抑制细胞外基质增生、聚集,减轻肾间质纤维化,延缓肾脏损害,其作用优于单独应用血管紧张素转化酶抑制剂。结论 AngⅡ和PDGF-B参与肾小管间质纤维化改变。
Objective To investigate whether benazepril combined with pancreatic kininogenase（PK） has protective effect on the kidney of rats with experimental renal tubulointerstitial fibrosis,and to explore the potential action mechanism.Methods 60 SD rats were randomly divided into sham-operation group（group A）,model group（group B）,benazepril treatment group（group C）,benazepril combined with PK treatment group（group D）.The pathological changes of renal tissues,the expression of angiotensin Ⅱ（AngⅡ） and platelet derived growth factor-B（PDGF-B）were observed for all the groups.Results The benazapril combined with PK could significantly decrease the content of AngⅡ（P0.05）,and could downregulate the expression of PDGF-B（P0.05）,which could inhibit the proliferation and accumulation of extracellular matrix,relieve renal tubulointerstitial fibrosis and renal injury,whose effect was superior to that of using simple angiotensin-converting enzyme inhibitor.Conclusion AngⅡ and PDGF-B are involved in the changes of renal tubulointerstitial fibrosis.
出处
《河北医药》
CAS
2011年第6期812-815,共4页
Hebei Medical Journal
