特发性肺纤维化( idiopathic pulmonary fibrosis，IPF)是一种病因不清、机制未明的弥漫性肺间质疾病，最终导致不可逆的呼吸功能衰竭，严重危害人类健康，目前尚无确定有效的治疗方法和药物。我们前期研究发现落新妇苷酚羟基衍生物具有抗IPF的作用，能够促进肺泡上皮细胞的损伤修复，初步明确可能与影响端粒稳态相关。本课题拟采用BLM/TGF-β1诱发的体内外肺纤维化模型，从组织形态学、基因表达调控、基因信息学等方面，利用miRNA芯片、基因转染、基因干扰等技术研究落新妇苷酚羟基衍生物抗肺纤维化作用中对miR-101/138-EZH2-TERRA-TERT-端粒信号通路的调控机制，为将其开发为抗肺纤维化的一类新药提供理论依据，同时为将TERRA开发为肺纤维化疾病新的基因靶标提供重要的理论和技术支持。

Idiopathic pulmonary fibrosis,a diffuse pulmonary interstitial disease of unknown etiology, eventually lead to irreversible respiratory failure.The treatment for IPF is supportive, and there are currently no known therapies and drugs that alter its natural history. The previous results showed that a hydroxylated phenolic derivative of Astilbin has therapeutic effects on IPF and could improve alveolar epithelial regenerative capacity which may partly due to its ability to regulate telomere stability. The objectives of this study are to determine whether the effect of the hydroxylated phenolic derivative of Astilbin on IPF is related to its modulation of miR-101/138-EZH2-TERRA-TERT-telomere signaling pathway using miRNA chip,gene transfection, gene interference technology from the aspect of histomorphology, regulation of gene expression and bioinformatics. And all the results may provide a theoretical basis for not only developping the hydroxylated phenolic derivative of Astilbin as a first class new drug(lung fibrosis) but also making TERRA as a novel molecular target for treatment of lung fibrosis.