本项目在前期的研究基础上，着眼于慢性萎缩性胃炎发生、发展过程中的其中一条重要炎症反应通路--JAK-STAT，以MNNG自由饮水法同时配合饥饱相间诱导慢性萎缩性胃炎模型大鼠为研究对象，以假埋线为对照，多水平、多层次地系统观察穴位埋线对慢性萎缩性胃炎JAK-STAT炎症反应通路的调节效应，提出"穴位埋线调节JAK-STAT炎症转导通路是穴位埋线改善慢性萎缩性胃炎的作用途径之一，而JAK2/STAT3信号转导通路异常激活，是其发挥作用的关键分子机制"的科学假说。并通过严谨的实验设计和先进的实验技术，观察穴位埋线对慢性萎缩性胃炎的改善作用，并探讨其分子信号机制；研究结果将为穴位埋线改善慢性萎缩性胃炎、调节JAK2/STAT3转导通路提供强有力的科学证据，并为临床应用穴位埋线治疗慢性浅表性胃炎、慢性糜烂性胃炎和慢性萎缩性胃炎等炎症介导的消化系统相关疾病奠定坚实的理论基础。

On the basis of previous researchs,this study forcuses on the other important signaling pathways associated with inflammatory response of chronic atrophic gastritis - JAK-STAT（Janus kinase-signal transduction and transcription activator）. In this study, we use the model rats with chronic atrophic gastritis induced by drinking a certain concentration of MNNG with irregular diet as objects and Huangqi false catgut embedding as control, systematically observe catgut embedding therapy regulating effect of JAK-STAT signaling pathways associated with inflammatory response in chronic atrophic gastritis at multi-level, put forward the hypothesis that regulating JAK-STAT is one of the most important ways for catgut embedding therapy improving chronic atrophic gastritis, the key molecular mechanism of this way is the abnormal activation of JAK2/STAT3 signaling pathway. This hypothesis would be verified by rigorous experimental design and advanced experimental technology. The conclusions of this study would supply scientific evidence for catgut embedding therapy improving chronic atrophic gastritis and regulating JAK2/STAT3 signaling pathway supply steady theory for catgut embedding therapy on the diseases related to diseases of digestive system mediated by inflammation, such as chronic superficial gastritis, chronic erosive gastritis and chronic atrophic gastritis.