贵州医科大学学报

1998, (03) 3-5

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肾炎大鼠肾小球α-SMA表达与基质增生的关系
The Relationship of Glomerular α SMA Expression to Mesangial Matrix Proliferation in Rat with Nephrotoxic Nephritis

张国忠,桂华珍,郭兵,万昌武,杨林
Zhang Guozhong, et al Department of Pathophysiology, Guiyang Medical College

摘要(Abstract):

为了进一步了解肾小球α平滑肌肌动蛋白(αsmothmuscleactin,αSMA)的表达与肾炎发病时肾小球基质增生的关系,我们观察了大鼠肾毒血清肾炎(nephrotoxicnephritis,NTN)发病1~14d肾脏组织形态、肾功能、肾小球αSMA和血小板衍生的生长因子(plateletderivedgrowthfactor,PDGF)以及基质成分纤维连接蛋白(Fibronectin,FN)、胶原Ⅲ和Ⅳ型的表达,并对αSMA、PDGF及基质成分间进行相关性分析。研究显示,NTN第3天大鼠肾小球表达αSMA和PDGF,先于FN的表达和胶原Ⅳ型的增多。在NTN第7和14天,αSMA和PDGF表达增加,并且两者间及与FN和胶原Ⅳ型之间呈显著正相关。在NTN各时间点均未能在肾小球中检测出胶原Ⅲ型的存在。研究表明,注射抗血清引起的肾小球免疫损伤刺激肾小球系膜细胞表达αSMA是系膜细胞被激活后大量分泌基质的标志。系膜区PDGF的分泌进一步加强了系膜细胞αSMA的表达及基质增生。
Kidney histology, renal function, glomerular α smooth muscle actin (α SMA),Platelet derired growth factor(PDGF), fibronectin(FN),collagen Ⅲ and Ⅳ were detected in rat with nephrotoxic nephritis (NTN) form day 1 to day 14. The correlations between glomerular α SMA expression and mesangial matrix components as well as PDGF were analysed in order to understand further the relationship of glomerular α SMA expression to mesangial matrix proliferation. The results showed that α SMA and PDGF appeared in glomerulus of NTN on day 3 and preceded the appearance of glomerular FN and increase in glomerular collagen Ⅳ. More increaes in glomerular α SMA and PDGF which paralleled with FN and collagen Ⅳ was observed on day 7 and day 14 of NTN. No glomerular expression of collagen Ⅲ was noted in control or NTN rats at any points of time course. Our studies suggested that α SMA was a marker of matrix secretion form mesangial cell after its immuneinsult by nephrotoxic serum. The increase in PDGF in glomerulus enhanced glomerular α SMA expression and mesangial matrix proliferation.

关键词(KeyWords): 肾炎,α-平滑肌肌动蛋白,血小板衍生的生长因子,纤维连续蛋白,胶原,蛋白尿
nephritis; α smooth muscle actin; platelet derived growth factor; Fibronectin; collagen; proteinuria

Abstract:

Keywords:

基金项目(Foundation): 贵州省自然科学基金

作者(Author): 张国忠,桂华珍,郭兵,万昌武,杨林
Zhang Guozhong, et al Department of Pathophysiology, Guiyang Medical College

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DOI: 10.19367/j.cnki.1000-2707.1998.03.005

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