扩张型心肌病(DCM)病因和发病机制复杂，缺乏针对性的治疗方法；其与心脏淋巴管生成的内在关系未明，机制不清。课题组前期研究提示DCM心脏淋巴管生成障碍，中药扩心方能够有效干预，其机制可能与VEGFC/D-VEGFR3/NRP2反应轴通路失衡相关。本项目拟在前期研究基础上，应用阿霉素诱导DCM大鼠模型、tnnt2a突变斑马鱼DCM模型研究淋巴管生成障碍；VEGFR3/NRP2抑制诱导斑马鱼淋巴管损伤和影响人淋巴管内皮细胞增殖、迁移、成管模型，观察该反应轴通路分子基因蛋白表达的变化，以及中药扩心方干预效应。通过应用形态学、淋巴管造影、免疫组化、血清药理、RNAi技术、RT-PCR、Western-Blot等现代技术方法，从大鼠、斑马鱼、细胞、分子等不同水平开展研究，探讨DCM心脏淋巴管生成障碍作用机制及中药扩心方干预机制，为DCM防治提供新的理论基础和应用依据，有着重要的基础与应用价值。

The etiology and pathogenesis of Dilated cardiomyopathy(DCM) are very complicated, it also lacks of appropriate treatment so far.And the internal relationship between DCM and cardiac lymphangiogenes is still unclear. Our previous study suggests that DCM may lead to lymphangiogenesis disorder in the heart, which may be effectively mediated by Chinese Traditional Medicine Kuoxinfang. The underlying mechanism may be related to the axial of VEGFC/D-VEGFR3/NRP2.Based on the previous studies, this project would use doxorubicin induced DCM rat model, tnnt2a mutation zebrafish DCM model to study lymphangiogenesis disorders, and VEGFR3/NRP2 inhibitor induced lymphatic vessel damage in zebrafish and affects human lymphatic endothelial cell proliferation, migration, tube formation model, to observe the gene expression changes of the molecular pathway-related molecules of VEGFC/D-VEGFR3/NRP2 axis pathway, meanwhile, use the Traditional Chinese Medicine Kuoxinfang to explore its effect.By using a variety of methods, such as morphology, lymphangiography, immunohistochemistry, serum pharmacology, RNAi technology, RT-PCR, Western-Blot and so on,and using different models such as rats, zebrafish and cells we explore the mechanism of DCM leading to lymphangiogenesis disorder in heart and the intervention mechanism of Traditional Chinese Medicine Kuoxinfang, which provides a new theoretical foundation for DCM prevention and has important application value.