人类系膜增生性肾小球肾炎（MsPGN）发病率高，其肾组织免疫炎性病变是医学界一大难题。我们实验发现，MsPGN模型——大鼠Thy-1肾炎发病早期，其肾组织中有炎症因子（IL-23和IL-36α）生成和T细胞、Mφ浸润。鉴于具有乙酰转移酶活性的转录辅激活因子（PCAF）和转录因子（KLF4）均是Thy-1肾炎大鼠肾组织早期和体外用亚溶解型补体攻膜复合物（即sublytic C5b-9）刺激肾小球系膜细胞（GMC）诱导上调的共表达基因，故为了探讨sublytic C5b-9诱导上述炎性细胞因子的转录调控机制，本研究拟从体内和体外探索KLF4的作用及其PCAF乙酰化修饰该转录因子后对这些炎症因子基因转录的影响。旨在为揭示Thy-1肾炎大鼠生成炎症因子和炎性病变的分子机制（包括表观遗传学调控），并为今后防治人类MsPGN提供依据。

Human mesangial proliferative glomerulonephritis (MsPGN) is a disease with high incidence, and the immunologic inflammation leading to damages is a difficult problem of medical research field in the world. Our previous studies demonstrated that the production of pro-inflammatory cytokines (IL-23 and IL-36α) and infiltration of inflammatory T cells and macrophages were seen in the renal tissue of rats with Thy-1 nephritis (a model of MsPGN). Given that the transcription coactivator PCAF with acetyltransferase activity and transcriptional factor KLF4 were significantly co-upregulated both in the renal tissue of rat Thy-1 nephritis and in the glomerular mesangial cells (GMC) stimulated with sublytic C5b-9 complex, and in order to elucidate the mechanism of transcriptional regulation on production of the pro-inflammatory cytokines in the GMC upon sublytic C5b-9 stimulation, we attempt to explore the role of KLF4, including the effects of acetylated KLF4 on the gene transcription of these cytokines. The purpose of our study is to reveal molecular and epigenetic mechanism in the expression of pro-inflammatory cytokines and renal damage in the rat with Thy-1 nephritis, and further to provide an evidence for preventing and treating human MsPGN.