溃疡性结肠炎严重影响人类健康，发病机制不清。已有报道miR-155促进肠炎发生。我们首次发现：①miR-155促进雌性小鼠肠炎发生，但在雄性小鼠作用完全相反，与雌激素受体GPER1有关；② GPER1可通过PI3K/AKT磷酸化途径活化IL-6/Th17上调促进炎症。已知mTORC2为miR-155靶基因，可调控雌激素受体表达。我们提出假说：miR-155靶向mTORC2抑制GPER1的表达，并激活AKT磷酸化途径，启动IL-6/STAT3的转录与表达，诱导Th17细胞分化促进肠炎反应，该过程受机体雌激素负反馈调节。本课题拟通过对miR-155、GPER1进行表达干预，运用流式、WB、定量PCR等技术，观察miR-155/GPER1轴对炎症调控作用，本研究将从全新的角度和思路阐明“miR-155/GPER1轴”的作用模式，并为溃疡性结肠炎治疗提供新靶点。

The pathogenesis of Ulcerative Colitis which affects human health is unclear. It has been reported that miR-155 promotes enteritis. We first found that ①miR-155 in female mice is proinflammatory, but on the contrary in male mice, ②GPER1 can activate PI3K/AKT phosphorylation pathway to improve expression of IL-6 and thus induce Th17 differentiation. mTORC2 which is the target gene of miR-155 can regulate the expression of estrogen receptor.We hypothesis miR-155 inhibits the expression of GPER1 through mTORC2 and activates AKT phosphorylation pathway, start transcription and expression of IL-6/STAT3, promote Th17 cell differentiation, regulate enteritis reaction, and the process is affected by the negative feedback regulation of organism estrogen. This study aim at adopting interfering expression of GPER1 and miR-155 in the animal model, observe the regulation of miR-155/GPER1 axis to inflammation by using Flow Cytometry, WB, quantitative PCR technology. This study will elucidate, from new perspective and insight, the role model of miR-155/ GPER1 axis and provide a new target for the treatment of enteritis treatment.