NLRP3炎症小体的活化致促炎因子表达上升，在溃疡性结肠炎(UC)免疫发病中占有重要地位。靶向调控NLRP3的活性具有抗UC的作用。NLRP3炎症小体是通过活性氧物质（ROS）途径激活，进而分泌促炎因子IL-1β、IL-18和IL-33。IL-1β还可通过自分泌和旁分泌途径激活NF-κB通路，分泌IL-1β、TNF-α、IL-6、IL-8等细胞因子，放大并形成失控性炎症反应，从而引起UC。前期研究表明，雷公藤多苷具有抑制炎症因子的表达及治疗UC的作用，但其作用机制及作用关键环节尚不清楚。我们推测，雷公藤多苷可能通过调控NLRP3炎症小体的活性发挥作用。而本项目将采用流式细胞术、免疫组化技术、siRNA干扰或基因敲除等方法深入地研究雷公藤多苷对促炎因子表达的影响，对NLRP3炎症小体的活性影响，以明确雷公藤多苷抗UC的作用机制。

The NLRP3 inflammasome activation induced proinflammatory cytokine expression rise, in ulcerative colitis (UC) plays an important role in the immunological pathogenesis. Targeted expression of NLRP3 activity with anti UC effect. The NLRP3 inflammasome by reactive oxygen species (ROS) pathway activation and secretion of proinflammatory cytokines, IL-1 β, IL-18 and IL-33. IL-1 β can also through autocrine and paracrine activation of NF- κ B pathway, secretion of IL-1 β, TNF- α, IL-6, cytokines such as IL-8, amplification and the formation of uncontrolled inflammatory reaction, resulting in UC. Previous studies have shown that, tripterygium glycosides with expression and treatment of UC inhibits cytokine role, but the key links of the mechanism of action and the effects is not clear. We speculate that, Tripterygium Glycosides may play a role by regulating the NLRP3 inflammasome activity. This project will use flow cytometry, immunohistochemistry, siRNA interference or knockout of Lei Gongteng were on the expression of inflammatory factor in promoting the in-depth, effect on the NLRP3 inflammasome activity, the mechanism is clear by tripterygium glycosides anti ulcerative colitis.

NLRP3炎症小体的活化致促炎因子表达上升，在溃疡性结肠炎(UC)免疫发病中占有重要地位。靶向调控NLRP3的活性具有抗UC的作用。NLRP3炎症小体是通过活性氧物质（ROS）途径激活，进而分泌促炎因子IL-1β、IL-18和IL-33。IL-1β还可通过自分泌和旁分泌途径激活NF-κB通路，分泌IL-1β、TNF-α、IL-6、IL-8等细胞因子，放大并形成失控性炎症反应，从而引起UC。本项目将采用流式细胞术、免疫组化技术、siRNA干扰或基因敲除等方法深入地研究雷公藤多苷对促炎因子表达的影响，对NLRP3炎症小体的活性影响，以明确雷公藤多苷抗UC的作用机制。