基于解痉多肽表达化生探讨ciRS-7/miR-7在胃癌前病变证候演变中的作用机制

胃癌前病变（PLGC）是胃癌二级预防的重要内容，其关键病理环节解痉多肽表达化生（SPEM）与幽门螺杆菌（Hp）的关系体现了PLGC主要病机“湿、毒、虚、瘀”所致的证候演变特征。前期研究发现Hp感染下脾胃虚实证候演变与Th1/Th2细胞平衡相关，miR-7间接调节Th1细胞在PLGC发展过程中为抑癌基因，预实验提示miR-7调节脾胃虚实证候演变中SPEM的进展，及文献提示ciRS-7抑制miR-7活性，但ciRS-7/miR-7在PLGC证候演变中的作用机制尚不明确。本课题通过国际公认的SPEM模型与现有的证候模型有机结合，分别复制“湿、毒、虚、瘀”病证结合的动物模型，观察不同证候与PLGC相互作用、与炎症因子的关系及对胃黏膜病变的影响，阐明ciRS-7/miR-7介导PLGC证候演变的作用靶点及分子机制。本课题拓宽了中医药研究PLGC的思路及方法，为中医药防治该病变奠定了理论和实验基础。

The prevention of precancerous lesions of gastric cancer (PLGC) is the main content of secondary prevention of gastric cancer. And dampness, toxin, deficiency and blood stasis are considered to be the major pathogenesis of PLGC, whose key pathology is spasmolytic polypeptide-expressing metaplasia (SPEM) . The relationship of SPEM and helicobacter pylori (Hp) gives a clue of characteristics of syndrome evolution by the major pathogenesis of PLGC. The prior clinical research results show that the syndrome of spleen stomach dampness heat and spleen Qi deficiency are related to the homeostasis of Th1 and Th2 cells, and microRNA-7(miR-7) is a tumor suppressor for PLGC by indirectly regulating the expression of Th1 cells. Furthermore, the advance experiment results of this research prove that the potential regulation property of miR-7 in the different syndrome of deficiency and solid spleen and stomach, with the literature results of inhibition of ciRS-7 for miR-7, however, the mechanism of ciRS-7/miR-7 in syndrome evolution of PLGC is unclear. In this research, the international generally accepted model of SPEM will combine with pre-existing syndrome model, with combination of disease and syndrome mouse model for dampness, toxin, deficiency and blood stasis independently. The relationship of syndrome and PLGC, cytokines and the influence for gastric mucosa lesions will be observed, in order to explain the target and molecule mechanism of ciRS-7/miR-7 mediated the syndrome evolution of PLGC. This research extends the thought and method of Chinese medicine for PLGC, and lays a theory and experiment foundation for the prevention of PLGC.