胃食管反流病（GERD）是消化系统常见疾病，反流导致的食管炎症为其重要病理特征,IL-8即是GRED患者食管慢性炎症中特征性介质之一。消退素D1（RvD1）是新发现的特异性促炎症消退脂质，可由食物中摄入的二十二碳六烯酸（DHA）氧化生成，其在GERD中的作用目前尚无研究。我们预实验发现RvD1在GERD大鼠食管中含量明显下降，体外实验证实RvD1能通过甲酰肽受体（FPR）2减少胰酶刺激的人食管上皮细胞中IL-8的表达，提示RvD1在GERD的发生和治疗中具有作用。下一步我们将在多个层面（细胞、动物模型、人体标本），采用荧光素酶报告基因、免疫共沉淀、qPCR、Western-blot等研究手段，系统研究RvD1在GERD炎症过程中的作用，并明确其作用的具体机制。本研究聚焦于功能性脂质分子对GERD的作用，有助于深入阐释GERD的发病机制，并为发掘GERD新的治疗方法和膳食建议提供理论基础。

Gastroesophageal reflux disease (GERD) is a common disease of the digestive system. Esophageal inflammation caused by reflux plays an important role in GERD pathology. IL-8 is one of the characteristic mediators of chronic inflammation in esophagus of patients with GRED. Resolvin D1 (RvD1) is a newly discovered specialized pro-resolving lipid mediators that could be produced by oxidation of Docosahexaenoic Acid (DHA) ingested in food, and its role in GERD has not been studied. We preliminarily found that RvD1 was significantly decreased in the esophagus of GERD rats and confirmed that RvD1 could reduce the expression of IL-8 in human esophageal cells stimulated by trypsin through Formyl Peptide Receptor (FPR)2, suggesting that RvD1 has a role in the pathogenesis and therapeutic treatment modality of GERD. Next, we will study the role and specific mechanisms of RvD1 in GERD inflammation systematically at various levels (cells, animal models, human specimens) , using different research methods including luciferase reporter gene, co-immunoprecipitation, qPCR, Western-blot, etc. The role of the functional lipid molecules in GERD will be focused during the study, which would help to interpretate the pathogenesis of GERD and provide a theoretical basis for discovering new treatments and dietary recommendations in GERD.