·糖尿病基础研究·

　　【摘要】 目的 观察不同浓度非诺贝特对高糖培养的足细胞的影响，探讨糖尿病肾病(DN)的早期机制。 方法 分离收集大鼠肾小球并进行足细胞原代培养。分别以正常糖(NG)组，高糖(HG)组，非诺贝特F50(50 μmol/L)、F100(100 μmol/L)、F200(200 μmol/L)组，继续培养48 h，观察足细胞形态变化，WB法半定量检测nephrin表达水平。 结果 与NG组比较，HG组足细胞逐渐出现足突回缩，部分足突消失及失去细胞间连接;nephrin表达量下降(P<0.05)。与HG组比较，F50和F100组可使足细胞足突恢复，上调足细胞nephrin表达量(P<0.05);F200组使足细胞损伤严重，足突消失，数量减少，抑制足细胞nephrin表达，与F50、F100组比较差异有统计学意义(P<0.05)。 结论 高糖引起足细胞损伤可能是DN的早期机制，非诺贝特激活PPAR-α后对高糖培养的足细胞有保护作用。

　　【关键词】 足细胞;高糖;PPAR-α激动剂;非诺贝特;糖尿病肾病

Influence of fenofibrate on expression of nephrin in primary cultured rat podocytes under high glucose Jia Miao, Zhang Yi-min , Xu An-ping, et al. Department of Nephrology, Postgraduate Student of Sun Yet-sen Memorial Hospital, Guangzhou 510655, China

Corresponding author: LAI De-yuan,E-mail: laideyuan2010@163.com

　　【Abstract】Objective To explore the influence of fenofibrate on glomerular podocytes cultured under high glucose to study the mechanism of chronic kidney disease in diabetes in the early stage. Methods The rat glomeruli were isolated and gathered for primarily culture. The cells were randomized into normal glucose (NG) group, high glucose (HG) group, fenofibrate 50μmol/L (F50) group, fenofibrate 100 (F100) group, and fenofibrate 200 (F200) group. The culture was continued for 48h. The morphological changes of podocytes were observed. The expression of nephrin was determined with Western Blot method. Result Compared with the NG group, the podocytic-process retraction and partial effacement and intercellular junction losing appeared in the HG group, the expression of nephrin was lowered (P<0.05). Compared with the HG group, there was a recovery of podocytic-process and up-regulation of expression of nephrin in the F50 and F100 groups (P<0.05). In the F200 group, there was a severe damage of the podocytes, including the podocytic-process decrease, even disappearance, and inhibited expression of nephrin, with a statistically significant difference from that of the F50 and F100 groups (P<0.05). Conclusion Damage of podocytes caused by high-glucose may be the mechanism of chronic kidney disease in diabetes in the early stage. Fenofibrate protects podocytes by activating PPAR-α.

　　【Key words】Podocyte; High glucose; PPAR-α agonist; Fenofibrate; Chronic kidney disease in diabetes