南方医科大学学报 ›› 2013, Vol. 33 ›› Issue (07): 1022-.

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11R-VIVIT抑制脂多糖诱导的足细胞尿激酶型纤溶酶原激活剂受体的表达

李锐钊,史伟,马娟,章斌,张丽,梁馨苓,陈源汉,刘双信,王文健   

  • 出版日期:2013-07-20 发布日期:2013-07-20

11R-VIVIT inhibits the expression of urokinase-type plasminogen activator receptor in podocytes

  • Online:2013-07-20 Published:2013-07-20

摘要: 目的观察11R-VIVIT对脂多糖诱导的足细胞尿激酶型纤溶酶原激活剂受体(uPAR)表达的影响。方法分别建立脂多糖
诱导小鼠蛋白尿模型和脂多糖诱导足细胞损伤模型,两种模型均分为正常对照组、脂多糖组和脂多糖+11R-VIVIT组。通过测
量尿蛋白—尿肌酐比值观察各组小鼠尿蛋白的情况;通过免疫荧光激光共聚焦,RT—PCR及Western blot 观察各组小鼠肾组织
及足细胞uPAR基因及蛋白水平。结果脂多糖组小鼠尿蛋白—尿肌酐比值高于正常对照组(P<0.001)及脂多糖+11R—VIVIT
组(P<0.001);脂多糖+11R—VIVIT组的小鼠肾组织及足细胞的uPAR的荧光表达弱于脂多糖组,但与正常对照组相似;足细胞
脂多糖+11R—VIVIT组的uPAR mRNA和uPAR蛋白表达均低于脂多糖组(PuPAR mRNA<0.001;PuPAR=0.001),但与正常对照组相类
似(PuPAR mRNA=0.095;PuPAR=0.252)。结论11R—VIVIT可能通过抑制足细胞uPAR的表达、稳定和保护足细胞从而起到降蛋白尿
的作用。

Abstract: Objective To observe the effect of 11R-VIVIT on lipopolysaccharide (LPS)-induced expression of urokinase-type
plasminogen activator receptor (uPAR) in podocytes. Methods A LPS-induced proteinuria mouse model and in vitro cultured
podocytes treated with LPS were both divided into control group, LPS group and LPS+ 11 R-VIVIT group. The mRNA and
protein expressions of uPAR in mouse kidney tissues and the podocytes were measured by real-time qPCR, laser scanning
confocal microscopy and Western blotting. Results Compared with LPS group, LPS+11 R-VIVIT group showed a significantly
lowered urine albumin/creatinine ratio (P<0.001) and markedly reduced mRNA and protein expressions of uPAR (PuPAR mRNA<
0.001; PuPAR=0.001). Conclusion 11R-VIVIT can ameliorate proteinuria probably by decreasing the expression of uPAR in
podocytes.