肾间质纤维化(RIF)是各种慢性肾脏病进展至终末期肾病的共同通路和主要病理基础。已证实肾小管上皮细胞可通过Fas/FasL凋亡途径促进RIF。课题组前期在UUO大鼠模型蛋白质组学中筛选出显著差异蛋白Niban，并首次发现RIF患者、动物及细胞模型中，随着Niban表达降低，肾小管上皮细胞凋亡增加，Fas/FasL途径标志蛋白caspase8表达增多；Niban siRNA干预后，上述现象更显著。因此我们提出假说：Niban能通过Fas/FasL凋亡途径调控RIF。本课题组拟采用免疫共沉淀、质谱、转染质粒、肾静脉注射Niban过表达干预基因敲除小鼠等方法，从体内外实验两个层面分别观察Niban对Fas、FADD、caspase8的影响，证实Niban能调控Fas/FasL途径，并进一步寻找与Niban相互作用的结合蛋白。本课题将为Niban成为可能的RIF有效治疗靶点提供实验依据。

Renal interstitial fibrosis（RIF）is closely correlated with end stage renal disease. Renal tubular epithelial cells can promote RIF through apoptosis pathway of Fas/FasL. We screened out differential protein, Niban, in proteomics study of UUO rats. In turn, we found that expression of Niban decreased obviously in patients, animal and cell model of RIF, contrary to increasing apoptosis of renal tubular epithelial cells and caspase8 which was the marker protein of Fas/FasL. Transfecting siRNA of Niban increased phenomenon above. So we put forward the hypothesis that Niban can regulate RIF through apoptosis pathway of Fas/FasL. In order to confirm Niban can regulate pathway of Fas/FasL, and make sure the binding protein interact with Niban, we plan to observe impact of Niban on Fas, FADD and caspase8 through vivo and vitro experiments with methods of immune coprecipitation, mass spectrum, transfection plasmid and renal vein injection Niban overexpression intervention to gene knockout mice. This topic will provide experimental basis for Niban being the possible and effective therapeutic target in RIF.