子宫内膜异位症（内异症）是妇科的常见病与多发病，发病率逐年上升。疼痛是内异症治疗的关键，因此，阐明内异症疼痛的发生机制，是内异症目前研究的热点与难点。前期研究发现，内异症病灶可检测到与患者疼痛和月经周期相关的ATP高浓度和P2X3受体高表达，但机制不清。ATP和P2X3受体可能在雌激素调控内异症疼痛的形成和维持中发挥重要作用。本项目拟应用分子生物学、行为学以及全细胞膜片钳等技术检测内异症患者GnRHa干预前后病灶ATP含量与P2X3受体表达水平；构建内异症SD大鼠模型，建立离体子宫内膜细胞和DRG细胞培养模型，测定模型大鼠和模型细胞雌激素及相关因子干预前后病灶、DRG、脊髓背角和离体细胞ATP含量与P2X3受体表达变化以及疼痛生物学行为改变。探讨ATP和P2X3受体参与雌激素调节内异症疼痛信号转导中的关键作用，寻获内异症疼痛信号转导中的关键分子，为将来研制临床上能治疗内异症疼痛的靶向药物。

Endometriosis is a common gynecological disease with its incidence increasing yearly. Pain is the characteristic symptom of endometriosis, and the key to endometriosis treatment is pain. So to clarify the mechanism of endometriosis-associated pain is becoming hotspot in this field. Our previous studies found that adenosine triphosphate (ATP) content and P2X3 receptor expression levels in endometriotic lesions are increased in women with endometriosis, which are associated with pain and menstrual cycle, but the exact mechanism is still unclear. ATP and P2X3 receptor may play an important role in the process of formation and maintenance of endometriosis pains adjusted by estrogen. In this project, molecular biology, behavioral science and whole-cell patch clamp will be performed to measure ATP content and P2X3 receptor expression levels in the different lesions of endometriosis patients after GnRHa intervention; we will use the SD rat model of endometriosis as the in vivo model, and the culture of dorsal root ganglion (DRG) and endometrial cells as the in vitro model, measuring the changes of ATP content and P2X3 receptor expression levels in the lesions and DRG and spinal cord neurons as well as biological behavioral changes before and after different interventions by estrogen and the related factors, so as to investigate the key role of ATP and P2X3 receptor in signal transduction pathway of endometriosis-associated pain, find key molecules involving in endometriosis pain transduction pathway, and even provide more effective treatments for endometriosis-associated pain by using a molecular targeted therapy.