慢性炎症是阿司匹林所致小肠损伤出血的重要环节之一，HIF1α的长期高表达是炎症持续加重的关键分子基础。前期研究发现，阿司匹林肠溶制剂可上调小肠NF-κB及HIF1α表达，激活肠道炎症级联反应；三七总皂苷可抑制HIF1α表达，减轻阿司匹林导致的小肠炎症损伤。基于此，我们提出科学假说：三七总皂苷可抑制阿司匹林所致的小肠炎症级联反应，对小肠黏膜起到保护作用，这一作用与调控mTOR-HIF1α-MIF/ITF信号通路有关。本研究借助阿司匹林肠溶制剂致小肠损伤大鼠模型及HIF1α沉默表达的大鼠小肠上皮细胞构建实验体系，从大鼠便血情况、肠道血流、小肠炎症因子变化、电镜下小肠超微结构变化、小肠病理损伤情况及小肠上皮细胞增殖率、通透性、凋亡率变化观察疗效，从小肠mTOR、HIF1α、MIF、ITF基因及蛋白表达观察作用机制，明确三七总皂苷抑制小肠炎症级联反应的关键环节，为两药临床联用提供实验基础。

Chronic inflammation is one of the key links of small intestinal injury caused by aspirin. Long-term high expression of HIF1α is the key molecular basis for the continuous aggravation of inflammation. Our previous studies have shown that enteric-coated aspirin can up-regulate the expression of NF-κB and HIF1α in the small intestine, and activate the intestinal inflammatory cascade reaction. Panax notoginseng saponins (PNS) can inhibit the expression of HIF1α and reduce the inflammatory injury of small intestine induced by aspirin. Based on this, we propose a scientific hypothesis: Panax notoginseng saponins can inhibit the intestinal inflammatory cascade reaction induced by aspirin and protect small intestinal mucosa, which is related to the regulation of mTOR-HIF1α-MIF/ITF signal pathway. In this study, enteric-coated aspirin induced small intestinal injury rat model and HIF1α-silent rat small intestinal epithelial cells were used to construct an experimental system, to observe the hematochezia, intestinal blood flow, changes of inflammatory factors in small intestine, microscopic injury of small intestine, pathological change of small intestine and the changes of proliferation rate, permeability and apoptosis rate of intestinal epithelial cells. The expressions of mTOR, HIF1α, MIF and ITF genes and proteins in small intestine were also detected to explore the protective mechanism of PNS on small intestinal injury induced by aspirin, so as to provide experimental basis for combination of PNS and aspirin in clinic.