中枢卒中后疼痛（Central post stroke pain, CPSP）是一类最顽固的慢性中枢神经病理性痛，严重影响患者的生活质量。到目前为止，其发病机制依然不清。我们前期成功建立了丘脑出血性卒中后疼痛的大鼠模型，并发现神经炎症可能是其发病的关键因素。课题组最新的研究结果显示：CPSP大鼠脊髓内的警报素IL-33表达上调，伴随胶质细胞激活、神经元活化以及中枢敏化形成，而抑制IL-33/ST2信号轴能有效翻转大鼠的痛敏行为，提示警报素IL-33/ST2信号轴参与CPSP的发病。据此，我们提出假说“脊髓内IL-33在丘脑损伤后作为警报素大量合成并释放，作用于ST2受体，一方面激活胶质细胞诱发神经炎症，另一方面活化神经元引起中枢敏化，最终导致CPSP的发生与维持”。为论证该假说，本课题采用多种手段，从分子、细胞到动物水平展开研究，为阐明CPSP发病机制提供理论基础，更为临床防治提供新靶点。

Central post stroke pain (CPSP) is an intractable neuropathic pain, which severely affects the living quality of patients. To date, the underlying mechanisms remains unknown as the basic research is rare. We previously established thalamic hemorrhage-induced experimental CPSP and identified that neuroinflammation in the central nervous system (CNS) was a key factor in the pathogenesis. Our latest studies revealed that the alarmin IL-33 was significantly up-regulated in the spinal cord after thalamic hemorrhage, accompanying with glial activation, neuronal hyperactivity and central sensitization. And blocked of spinal IL-33/ST2 signaling could efficiently reverse the CPSP, suggesting a critical role of IL-33/ST2 signaling in the development and maintenance of CPSP. Based on these results, we hypothesized that spinal IL-33 was secreted as an alarmin once thalamus was injured and which induced neuroinflammatory reaction and central sensitization in the spinal cord through ST2 receptor, eventually resulting in the initiation and maintenance of CPSP. In the present study, we aim to explore the cellular and molecular mechanisms of CPSP by using multiple methods. It is expected to provide theoretic basis for the pathogenesis and new targets for the treatment of CPSP.