淋巴水肿患病人数逾2.5亿，且具有致死风险。然而，目前治疗方法有限且疗效欠佳，因此，研究新的治疗方法已成为临床实践中亟待解决的问题。近来，研究表明炎症既可导致淋巴水肿，又能加重其病理改变，而七叶皂苷具有抗炎作用，并可提高患者血清内降钙素基因相关肽（CGRP）浓度，同时CGRP/RAMP1/CLR信号通路可调控M1/M2型巨噬细胞比例，抑制淋巴水肿组织内炎症。申请人前期研究证实淋巴水肿组织内促炎因子浓度过高存在炎症状态，同时成功构建鼠尾淋巴水肿模型，并发现七叶皂苷抑制炎症可以缓解鼠尾淋巴水肿，具体机制尚未明确。本研究拟通过免疫荧光、FACS、PCR、蛋白芯片等技术，在体内和体外实验中，阐明七叶皂苷通过CGRP/RAMP1/CLR信号通路调控M1/M2型巨噬细胞比例，抑制淋巴水肿组织内炎症，进而缓解纤维化和水肿，促进淋巴管新生，实现治疗淋巴水肿的作用及其机制，为淋巴水肿的药物治疗提供新的选择。

Lymphedema has more than 250 million patients and is at risk of death. However, the current treatment methods are limited and the curative effect is not good. Researching new treatment methods has become an urgent problem in clinical practice. Recently, studies have shown that inflammation can cause lymphedema and aggravate pathological changes, and aescin has anti-inflammatory effects and can increase the concentration of calcitonin gene-related peptide (CGRP) in patients' serum. The CGRP / RAMP1 / CLR signals pathway can regulate the proportion of M1 / M2 macrophages and inhibit inflammation in lymphedema tissue. The applicant's previous research confirmed that there is an inflammatory state in the lymphedema tissue with high concentration of pro-inflammatory factors. At the same time, a rat tail lymphedema model was successfully constructed, and it was found that the inhibition of inflammation by aescin can alleviate rat tail lymphedema. The specific mechanism has not yet been determined. This study intends to use immunofluorescence, FACS, PCR, protein chip and other technologies to explain in vivo and in vitro experiments that aescin can regulate the proportion of M1 / M2 macrophages through the CGRP / RAMP1 / CLR signal pathway and inhibit lymphedema Inflammation, thereby alleviating fibrosis and edema, promoting lymphangiogenesis, realizing the mechanism of treatment of lymphedema, and providing new options for medical treatment of lymphedema.