慢性胰腺炎（CP）是一种迁延不愈、临床难治性疾病，晚期可进展为糖尿病、胰腺外分泌功能不全或胰腺癌，严重影响患者生活质量，其主要病理学特征是胰腺纤维化，但目前尚无有效干预措施。Erbin是最近发现的LAP家族重要成员，具有逆转TGF-β1诱导肾上皮细胞间质转化（EMT）作用，但对胰腺纤维化和EMT作用尚不清楚。我们前期研究成功构建了二丁基二氯化锡诱导CP纤维化动物模型并分离和原代培养了胰腺星状细胞（PSC），且发现CP患者血清及组织中erbin和TGF-β1显著上调。本研究拟通过RT-PCR、Western Blot和质粒转染等技术，证实TGF-β1可诱导PSC发生EMT，并明确erbin对TGF-β1诱导PSC发生EMT的抑制作用，同时检测Smad和ERK信号转导通路相关基因和蛋白表达，明确其调控胰腺纤维化及EMT的分子机制，丰富胰腺纤维化机制研究，为抑制或逆转胰腺纤维化提供新的治疗靶点。

Chronic pancreatitis(CP) is a clinical refractory disease with resistance to cure, when it reaches the advanced stage, the patients will present with diabetes, exocrine insufficiency or pancreatic cancer, which will affect their quality of life seriously. As we all know, pancreatic fibrosis is one of the most typical histopathological features, but there are not any effective treatments available for it. Erbin, as a new member of LAP family, has the capability to reverse the effects of TGF-β1 on the process of renal epithelial-to-mesenchyal transition(EMT). Whether erbin has a similar impact on pancreatic fibrosis and EMT is yet unknown. Before this, we have already estasblished animal models of CP induced by DBTC and mastered the skills of purifying and culturing pancreatic stellate cell(PSC) . Our preliminary study confirmed that the expression levels of erbin and TGF-β1 increased in both the serum and pancreatic tissue of CP patients. In this study, we will go further to prove that TGF-β1 could activate quiescent PSC and thus induce EMT by means of RT-PCR, Western Blot, recombinant plasmid and the like. We also want to make sure whether erbin can inhibit pancreatic EMT induced by TGF-β1 and do the research on the signal conducting pathway such as Smad and ERK. In a word, we aim to find out the modifying system of pancreatic fibrosis and the molecular mechanism of EMT, to diversify the pathogenesis of pancreatic fibrosis and to provide a new way for the treatment of CP.