基于夏氏外科“清热利湿通络法”治疗痛风的临床经验，在前期研究证实“清热利湿通络法”通过抑制中性粒细胞活化和向炎症部位趋化、聚集，同时减少炎症介质释放来拮抗痛风的基础上，结合Cyr61与免疫性疾病炎性微环境研究进展，课题组提出假说：“清热利湿通络法”拮抗痛风的关键环节与Cyr61/CCN1调控痛风炎性微环境密切相关。项目组采用在体和离体实验相结合，分别以尿酸钠悬浊液诱导大鼠痛风模型和正常大鼠及其FLS为研究对象，采用shRNA慢病毒颗粒、与Anti-Cyr61抗体共同孵育方法，明确Cyr61/CCN1作为一种新的炎症因子在痛风炎性微环境的形成及发病过程中的作用，探讨“清热利湿通络法”治疗痛风的细胞分子生物学机制及其内在规律，为将Cyr61蛋白作为“清热利湿通络法”治疗痛风的新靶点提供重要的理论依据和实验基础。

Based on the clinical experience of the XiaShi surgery treatment of gout by “Clearing heat and removing dampness and dredging collaterals method”, and our previous studies demonstrated “Clearing heat and removing dampness and dredging collaterals method”can inhibi neutrophil activation and chemotaxis to sites of inflammation、aggregation, and reduce the release of inflammatory mediators,combines the reserch progress of the relationship of Cyr61 and synovial inflammatory microenvironment, our research group hypothesized that:“Clearing heat and removing dampness and dredging collaterals method”antagonize gout’s key link has a very close relationship with Cyr61/CCN1 regulats inflammatory synovial microenvironment. This project uses the in vivo and in vitro experiments combining, respectively using sodium urate suspension induced rat model of gout、normal rats and their FLS for the study, using shRNA Lentiviral Particles and the expression method of Anti-Cyr61 antibody interference in Cyr61 to studied on the function of the Cyr61 in the gout inflammatory microenvironment and investigating “Clearing heat and removing dampness and dredging collaterals method” ’s cellular and molecular biological mechanisms as well as its internal regular pattern,to provide important theoretical basis and experimental basis for the Cyr61 protein as a new target for the treatment of gout by “Clearing heat and removing dampness and dredging collaterals method”.