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2型糖尿病肾病大鼠肾小管间质病变及TGF-β1、HGF和CTGF表达的变化及意义 被引量：12

Changes in Tubular-interstitial Pathomorphology and Expression of TGF-β1,HGF and CTGF in a Rat Model of Type 2 Diabetic Nephropathy
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摘要 目的通过2型糖尿病肾病(T2DN)大鼠模型,探讨早期糖尿病肾病(DN)肾小管间质的病理变化及转化生长因子β1(TGF-β1)、肝细胞生长因子(HGF)和结缔组织生长因子(CTGF)表达变化及意义。方法高热量饲料喂养加腹腔注射链脲佐菌素(STZ),复制T2DN模型。14周和20周时用HE染色及PASM染色方法观察肾小管及间质的病理变化;用免疫组织化学的方法观察肾小管间质中TGF-β1、HGF和CTGF的表达变化,并进行半定量分析。结果模型组大鼠具有血糖异常、胰岛素抵抗及肾小球高滤过率、白蛋白尿等特点;部分肾小管上皮细胞萎缩、脱落、空泡化,基底膜增厚及小管间质纤维化。免疫组织化学方法提示TGF-β1和HGF14周及20周时在2组大鼠小管间质的表达差异有统计学意义(P<0.01);CTGF在2组大鼠肾小管间质有少量表达,差异无统计学意义。结论早期DN大鼠模型中肾小管间质已开始出现纤维化改变;TGF-β1、CTGF和HGF在早期DN的肾小管及间质中的表达发生变化,提示TGF-β1、CTGF和HGF在肾小管间质的表达失衡与DN肾小管病变的进展相关。 Objective To develop a rat model of type 2 diabetic nephropathy and to investigate changes in tubular-interstitial pathomorphology and expression of TGF-β1,HGF and CTGF in early-stage diabetic nephropathy.Methods Forty-four eight-week-old male Wistar rats were fed a normal or high-energy(46% of total calories from fat) diet for 20 weeks,and at week 6 rats received once intraperitoneal injection of citric acid buffer or STZ(30 mg/kg).In the eighth week,two groups underwent intraperitoneal injection glucose t...
作者 安娜 刘惠兰 王英
机构地区 首都医科大学附属复兴医院肾内科
出处 《首都医科大学学报》 CAS 2008年第3期315-320,共6页 Journal of Capital Medical University
基金 北京市西城区科技创新基金(2007036)资助项目~~
关键词 2型糖尿病肾病 肾小管间质 转化生长因子 肝细胞生长因子 结缔组织生长因子 type 2 diabetic nephropathy tubular-interstitial transforming growth factor hepatocyte growth factor connective tissue growth factor
分类号 R692 [医药卫生—泌尿科学]
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参考文献17

  • 1[1]Caramori M L,Mauer M.Diabetes and nephropathy[J].Curr Opin Nephrol Hypertens,2003,12:273-282.
  • 2[2]Thomas M C,Burns W C,Cooper M E.Tubular changes in early diabetic nephtopathy[J].Adv Chronic Kidney Dis,2005,12:177-186.
  • 3[3]Liu Y.Epithelial to mesenchymal transition in renal fibogenesis:pathologic significance,molecular mechanism,and therapeutic intervention[J].J Am Soc Nephrol,2004,15:1-12.
  • 4[4]Cruzado J M,Lloberas N,Torras J,et al.Regression of advanced diabetic nephropathy by hepatocyte growth factor gene therapy in rats[J].Diabetes,2004,53:1119-1127.
  • 5[5]Morcos M,Sayed A A R,Bierhans A,et al.Activation of tubular epithelial cells in diabetic nephropathy[J].Diabetes,2002,51:3532-3544.
  • 6[6]Ziyadeh F N.Mediators of diabetic renal disease:the case for TGF-β as the major mediator[J].J Am Soc Nephrol,2004,15:S55-S57.
  • 7[7]Fraser D,Bruskill N,Ito T,et al.Long-term exposure of proximal tubular epithelial cells to glucose induces transforming growth factor-β1 synthesis via an autocrine PDGF loop[J].Am J Pathology,2003,163:2565-2574.
  • 8[8]Cohen M P,Ziyadeh F N,Hong S W,et al.Inhibiting albumin glycation in vivo ameliorates glomerular overexpression of TGF-β1[J].Kidney International,2002,61:2025-2032.
  • 9[9]Morrisey K,Evans R A,Wakefield L,et al.Translational regulation of renal proximal tubular epithelial cell transforming growth factor-β1 generation by insulin[J].Am J Pathology,2001,159:1905-1915.
  • 10[10]Lam S,van der Geest R N,Verhagen N A,et al.Secretion of collagen type IV by human renal fibroblasts is increased by high glucose via a TGF-TGF-β-independent pathway[J].Nephrol Dia Transplant,2004,19:1694-1701.

二级参考文献36

  • 1Ong AC, Fine LG. Loss of glomerular function and tubulointerstitial fibrosis: Cause and effect? Kidney Int,1994;45(2):345.
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  • 7Murphy M,Godson C,Cannon S, et al.Suppression subtractive hybridization identifies high glucose levels as a stimulus for expression of connective tissue growth factor and other genes in human mesangial cells.J Biol Chem,1999;274(9):5830.
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共引文献32

同被引文献188

引证文献12

二级引证文献44

首都医科大学学报
2008年 第3期

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