中文摘要：

目的：探讨miR-23b通过与靶基因ASK1作用对糖尿病肾病纤维化的影响。方法：通过建立动物模型（I型糖尿病小鼠）和细胞模型（HK-2细胞），应用实时定量荧光PCR、免疫荧光、基因转染结合RT—PCR，检测ASK1、FN、miR-23b在糖尿病组（Dia组）和正常组（Con组）（P〈0．001）表达变化及在mRNA和蛋白水平上的作用关系。结果：miR-23b在Dia组的表达低于Con组；ASK1、FN在Dia组高表达，并且ASK1在Dia组中持续高表达；过表达miR-23b可以同时在mRNA和蛋白水平上抑制ASK1，P38的表达，FN表达也显著降低。结论：miR-23b可能通过作用靶基因ASKl及其信号通路抑制糖尿病肾病纤维化。

英文摘要：

Objective：This study discusses miR -23b effects on diabetic nephropathy fibrosis through interacting with its target gene ASK1. Methods：By establishing the animal model（ diabetes type I mice ） and the cell mode （HK -2 cell）, application of real -time PCR,western blotting ,immunofluoresence staining and Con group and the changes in the mRNA and protein levels on the role of the relationship, were observed. Results：The level of miR -23b in Dia group compared to the level in Con group;Compared with Con group , the expression of ASK1, FN were increased in Dia group and ASK1 had continuous high expression in Dia group; Over - expression of miR -23b induced the expression of ASK1 and P38 at both mRNA and protein levels, and the expression of FN is significantly reduced. Conclusion：miR -23 b positively inhibit diabetic nephropathy fibrosis by regulating target genes ASK1 and signaling pathways.