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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。
Objective To investigate the effect of 11R-VIVIT on lipopolysaccharide-induced urokinase-type plasminogen activator receptor (uPAR) expression in podocytes. Methods Lipoprotein-induced mouse model of proteinuria and model of lipopolysaccharide-induced podocyte injury were established. The two models were divided into normal control group, lipopolysaccharide group and lipopolysaccharide + 11R-VIVIT group. Urinary protein-urinary creatinine ratio was used to observe urinary protein in each group. The expression of uPAR gene and protein in kidney and podocytes were observed by immunofluorescence confocal laser scanning confocal microscope, RT-PCR and Western blot. Results The urinary protein-urinary creatinine ratio in the lipopolysaccharide group was higher than that in the normal control group (P <0.001) and the lipopolysaccharide + 11R-VIVIT group (P <0.001) The expression of uPAR mRNA and uPAR protein in podocyte lipopolysaccharide + 11R-VIVIT group was lower than that in lipopolysaccharide group (PuPAR mRNA <0.001; PuPAR = 0.001 ), But similar to the normal control group (PuPAR mRNA = 0.095; PuPAR = 0.252). Conclusion 11R-VIVIT may play a role in reducing proteinuria by inhibiting the expression of uPAR in podocytes, stabilizing and protecting podocytes.