全基因组miRNA筛选发现，AGS细胞转染miR-1224-5p后，由Hp感染诱发的NF-κB通路下调;SIN3A是miR-1224-5p的重要靶基因之一。RNAi沉默SIN3A可特异性抑制由Hp激活的NF-κB通路。SIN3A对H3K27去酰基化和基因转录起重要作用，且SIN3A及miR-1224-5p在多种肿瘤细胞系中呈差异表达。但miR-1224-5p及SIN3A对Hp感染诱导NF-κB信号通路激活及其疾病相关性尚未见报道。本研究拟借助细胞、分子、组织样本及动物模型，分析miR-1224-5p及SIN3A在胃上皮细胞和Hp感染不同病变胃粘膜中的动态表达，研究其与NF-κB激活的关系，探讨miR-1224-5p及SIN3A在Hp感染起始阶段如何通过影响H3K27Ac及其靶基因启动子的活性来激活NF-κB，将为Hp感染相关疾病的诊断与防治寻找新标志物与有效靶点提供理论依据。

We found from a genome-wide microRNA screen that, three days post transfection of miR-1224-5p into AGS cells，the NF-κB activation induced by H.pylori infection was abrogated significantly. SIN3A is predicted to be a potential target gene of miR-1224-5p.RNAi silencing of SIN3A could specifically inhibit the NF-κB signal pathway activated by H.pylori infection, instead of induction by TNFα or IL1β. It was shown that SIN3A is a key regulator of deacetylation of H3K27 and plays important roles in gene regulation，and the expression level of miR-1224-5p and its target gene SIN3A in various cancer cell lines is significantly high and low, respectively.However, there is no evidence about the functions miR-1224-5p and its target gene SIN3A play during the NF-κB signal pathway activated by H.pylori infection and the progression of related gastric diseases.Therefore, from different levels of cell cultures, molecular mechanisms, clinic tissue samples and animal model, we proposed here by applying diverse in vitro and in vivo experimental techniques, to investigate the dynamic expression level of miR-1224-5p and its target gene SIN3A in gastric epithelial cell lines and clinic tissue samples in different phases of H.pylori infection related diseases, to reveal how they are involved in the NF-κB signal pathway activated by H.pylori infection，and to study the molecular mechanisms on how miR-1224-5p and SIN3A play specific roles in NF-κB activation by affecting H3K27Ac and subsequently the activity of the promoters of the target genes of SIN3A. The completion of this project will aid in understanding the initiation and development of H.pylori infection related gastric diseases, pave the way for better diagnostics and treatment, and provide theoretic basis for searching for novel marker and effective targets.