类风湿性关节炎（RA）是一种滑膜细胞凋亡异常的自身免疫性疾病，在前期研究当归拈痛汤能够抑制RA-FLS致炎效应，保护关节滑膜的基础上，体外预实验发现并验证LncRNA NR_028371及多个效应分子参与调控滑膜细胞促凋亡蛋白Fas，因此本项目提出如下假说：当归拈痛汤作用于RA-FLS，通过上调NR_028371影响靶基因Fas表达水平，继而激活NR_028371-Fas细胞凋亡通路，从而诱导细胞凋亡、抑制细胞增殖。本项目拟从细胞、动物模型、临床水平对上述假说进行验证，旨在探讨当归拈痛汤调控NR_028371/Fas信号通路的作用机制，以期阐明当归拈痛汤诱导凋亡作用的非编码RNA新机制，为全面诠释当归拈痛汤诱导RA滑膜细胞凋亡的分子机制提供实验依据，从而丰富当归拈痛汤F防治RA的疗效机理，亦为RA现代药理基础研究拓宽思路。

Rheumatoid arthritis (RA) is a kind of autoimmune disease with abnormal apoptosis of synovial cells.Based on the earlier research that DangGuiNianTongTang can inhibit the induced inflammatory effect of RA-FLS and protect the synovium of joint, pre-vitro experiment has discovered and verified that LncRNA NR_028371 and multiple effector molecules participate in regulating synovial cell pro-apoptotic protein Fas,so this project proposes the following hypothesis:DangGuiNianTongTang acts on RA-FLS,influences Fas protein expression levels of target gene by upregulating NR_028371, then activates NR_028371-Fas cell apoptosis pathways to induce cell apoptosis and inhibit cell proliferation.The program intends to verify the above hypothesis in the level of cells,animal models and clinical characteristics,which is aimed to discuss the mechanism of action that DangGuiNianTongTang regulates NR-028371/Fas signal pathways and its effector molecules.We are hoping to illuminate the new and noncoding RNA mechanism that DangGuiNianTongTang induces apoptosis,providing experimental basis for the molecular mechanism of interpretating comprehensively that DangGuiNianTongTang induces cell apoptosis of RA synovial cells.The therapeutic effects’ mechanism of DangGuiNianTongTang will be enriched and thingking fields of RA modern pharmachological basis study can be broaden.