JAK/STAT通路是引起溃疡性结肠炎（UC）的关键通路，具体机制尚未完全明确。黄连解毒汤（HLJD）具有UC治疗作用，能下调炎症因子水平。基于此发现，本研究拟建立葡聚糖硫酸钠（Dsextran sulphate sodium，DSS）诱导的小鼠UC模型，采用定量PCR、Western blot等技术，测定IL-1、IL-6、TNF-α等因子水平，测定JAK/STAT通路中p-STAT1、p-STAT3蛋白表达的变化，测定凋亡调控因子Bcl-2、Bcl-x1、Bax的基因和蛋白表达以及Caspase-3活性，阐明JAK/STAT信号通路UC发病过程中的激活规律及对凋亡调控因子的影响。此后，观察分别应用JAK/STAT通路阻断剂和HLJD干预后上述指标的变化情况，评价该通路对UC的治疗价值，揭示HLJD治疗UC的机制。本研究对于UC药物新靶标的发现及HLJD治疗UC分子机制，具有重大意义。

JAK/STAT pathway is one of the key pathways to produce UC, but the mechanism is not completely clear. Based on the previous research, Huanglian Jiedu Decoction (HLJD) has significant therapeutic effects of UC, can down-regulate the level of inflammatory cytokine in UC mice. Based on the previous findings, this project is planning to duplicate UC induced by dextran sulfate sodium (DSS) in mice, and than to detect the levels of IL-1, IL-6,TNF-alpha and activity of caspase-3, to evaluate the protein and gene expressions of p-STAT1, p-STAT3, Bcl-2, Bcl-x1, Bax via quantitative PCR and Western blot. It is aim to clarify rules of to the JAK/STAT signaling pathway in the pathogenesis of UC and influence on apoptosis regulating factor. After that, JAK/STAT signal pathway blocking agent and HLJD will be administrated to intervene the pathway in order to evaluate the therapeutic value of the pathway for UC, to explore the mechanism of HLJD in the treatment of UC. This research will exhibit important significance in exploring the new target of drugs in UC, and revealing the molecular mechanism of HLJD in treating UC.