实验性慢性肾缺血中肾小管-间质细胞表型转化的规律及意义  

Role of cell phenotypic change in tubules and interstitium in experimental chronic renal ischemia

作　　者：贺巍[1] 陈威[1] 刘彦仿[1] 王川[1] 

机构地区：[1]第四军医大学西京医院肾脏内科,陕西西安710032

出　　处：《西北国防医学杂志》2003年第4期286-288,F003,共4页Medical Journal of National Defending Forces in Northwest China

摘　　要：目的 :研究Goldblatt肾动脉狭窄 (RAS)大鼠模型中慢性缺血肾脏肾小管 -间质细胞表型转化的规律及意义。方法 :制备RAS大鼠模型 ,用免疫组化方法观察α -平滑肌肌动蛋白 (α -SMA)、波型蛋白 (Vimentin)、转化生长因子 β1 (TGF - β1 )在肾小管间质中的表达变化规律及其与肾小管间质损伤的关系。结果 :RAS术后α-SMA、Vimentin、TGF - β1 在肾小管间质中的表达均增高 ;α -SMA及Vimentin的表达同肾间质纤维化的程度均为正相关 (r =0 .82 3,P <0 .0 1 ;r=0 .785 ,P <0 .0 1 )。结论 :肾小管-间质细胞表型转化是促进缺血后肾间质纤维化发展的重要因素 ,αObjective: To explore the role of cell phenotypic change in tubules and interstitium involved in the development of ischemic renal atrophy induced by renal artery stenosis(RAS). Methods:Rats were sacrificed at different time point after RAS or sham-surgery and the protein expressions of α-smooth muscle actin(α-SMA),Vimentin, transforming growth factor-β 1(TGF-β 1) were detected by immunohistochemistry at each time point.Results: All the protein expressions of α-SMA, Vimentin and TGF-β 1 in renal tubulointerstitium increased progressively after RAS. Both the expressions of α-SMA and Vimentin were significantly associated with the degrees of tubulointerstitial fibrosis. Conclusion: Purely chronic ischemia of kidney could result in progressive tubulointerstitial fibrosis, and cell phenotypic transformation in tubules and interstitium may play an important role in this process. α-SMA and Vimentin may be the early markers of chronic ischemic renal tubulointerstitial fibrosis.

关 键 词：肾疾病 缺血 纤维化 α—平滑肌肌动蛋白 波型蛋白 

分 类 号：R692.9[医药卫生—泌尿科学]