UC以肠道炎症、黏膜损伤为特点，止血与促溃疡愈合是治疗关键。蛋白质组学实验发现UC小鼠结肠RSK1、TSC2等蛋白异常表达，雷帕霉素加重黏膜损伤，龙血竭促进黏膜愈合，机制未明。我们提出假说:龙血竭可能通过干预RSK1-TSC2-mTOR信号轴调控黏膜愈合相关蛋白的表达、自噬水平促进UC小鼠肠黏膜修复。本项目先通过UPLC-QTOF-MS技术测定入血成分，采用网络药理学探讨龙血竭的作用机制；然后，通过蛋白质组学和血清代谢组学检测UC小鼠及龙血竭干预后的差异蛋白和代谢物，寻找并验证潜在蛋白靶标和代谢标志物；最后，探讨RSK1-TSC2-mTOR信号轴对结肠黏膜愈合相关蛋白和自噬水平的调控机制，以及龙血竭的干预作用及机制。本项目采用蛋白质组学和代谢组学技术系统、整体地研究UC发生发展过程中靶点、通路和代谢过程的变化，以及龙血竭的干预及其药效物质，并寻找潜在靶标和代谢标志物，具有重要临床意义。

UC is characterized by intestinal inflammation and mucosal injury. Hemostasis and ulcer healing are the key points of treatment. Proteomic experiments showed that RSK1, TSC2 and other proteins were abnormally expressed in UC mice colon, rapamycin aggravated mucosal injury, Chinese Dragon's Blood promoted mucosal healing, and the mechanism was unclear.We hypothesize that Chinese Dragon's Blood may promote intestinal mucosal repair in UC mice by interfering with RSK1-TSC2-mTOR signal axis to regulate the expression of mucosal healing-related proteins and autophagy levels.In this project, the blood components were determined by UPLC-QTOF-MS technology, and the mechanism of Chinese Dragon's Blood was explored by network pharmacology.Then, differential proteins and metabolites were detected by proteomics and serum metabolomics after intervention of UC mice and Chinese Dragon's Blood, and potential protein targets and metabolic markers were identified and validated.Finally, we discussed the regulation mechanism of RSK1-TSC2-mTOR signal axis on colonic mucosal healing-related proteins and autophagy levels, and the intervention effect and mechanism of Chinese Dragon's Blood.This project uses proteomics and metabonomics technology to systematically study the changes of targets, pathways and metabolic processes during the occurrence and development of UC, as well as the intervention of Chinese Dragon's Blood and its pharmacodynamic substances, in order to find potential targets and metabolic markers, which have important clinical significance.