血管新生是子宫内膜异位生长导致子宫内膜异位症的必经阶段。清热化瘀法能够抑制异位内膜组织增生，导致其萎缩，但具体作用机制不清。我们的前期工作发现清热化瘀法治疗EMs的过程伴随VEGFA及其受体KDR在异位内膜中表达显著降低，血管新生受到抑制。据此我们提出假说，清热化瘀法治疗EMs可能是通过VEGFA/KDR信号通路影响PTGS2活性，下调巨噬细胞PGE2的分泌，进而下调异位内膜雌激素的分泌，抑制血管新生而阻止异位内膜生长。我们采用常规分子生物学方法与芯片技术结合的方案，研究清热化瘀法调控VEGFA/KDR信号通路，抑制大鼠EMs模型异位内膜组织血管新生的机制，筛选其信号通路中的生物标志物，用于监测临床患者治疗前后该通路的变化，以便探索清热化瘀法治疗EMs的作用机制，寻找药物的作用靶点，并筛选可应用于临床诊断与治疗的新指标。

Angiogenesis is the necessary phase in endometriosis caused by endometrial ectopic growth. Clearing heat and removing blood stasis can inhibit the hyperplasia of ectopic endometrium tissue, causing them to atrophy, but the specific mechanism is unclear. Our previous study showed that the expression of VEGFA and its receptor KDR in ectopic endometrium was obviously decreased in the process of clearing heat and removing blood stasis treatment for EMs, and angiogenesis was restrained. Accordingly, we put forward the hypothesis that clearing heat and removing blood stasis treated EMs may be through VEGFA/KDR signaling pathway that affect PTGS2 activity, reduce the secretion of PGE2 in macrophages, and then decline the estrogen secretion in ectopic endometrium, thereby inhibit angiogenesis and prevent the growth of ectopic endometrium. We will use conventional techniques of molecular biology and chips to study the mechanism of clearing heat and removing blood stasis to regulate VEGFA/KDR signaling pathway and to inhibit angiogenesis in ectopic endometrium in the EMs rat models. We will select biomarkers in the signaling pathway to monitor the change of the pathway before and after treatment on clinical patients, in order to explore the mechanism of clearing heat and removing blood stasis treated EMs, looking for the drug targets, and screening the new biomarkers can be applied to clinical diagnosis and treatment.