基于转录组学联合N6-甲基腺嘌呤（N6-Methyladenosine, m6A）筛选类风湿关节炎（rheumatoid arthritis, RA）基因及化合物Q-1的干预进行研究。复制大鼠胶原诱导关节炎模型，检测各组大鼠血清中肿瘤坏死因子-α （tumour necrosis factor-alpha, TNF-α）、白细胞介素-6 （interleukin 6, IL-6）、白细胞介素1β （interleukin1β，IL-1β）的含量。转录组测序分析踝关节组织差异基因，对差异基因进行信号通路分析。将RA差异表达基因和26个m6A系统基因进行交集分析，对锌指CCCH型含13（zinc finger CCCH domain-containing protein 13, ZC3H13），胰岛素样生长因子结合蛋白2（insulin- like growth factor binding protein 2, IGFBP2）进行受试者工作特征曲线（receiveroperating characteristic curve, ROC）分析，采用分子对接分析化合物Q-1与ZC3H13，IGFBP2的结合情况。与正常对照组比较，模型组大鼠血清中TNF-α、IL-6、IL-1β的含量明显升高（P < 0.01）。与正常对照组相比，模型组共鉴定出1 300个差异基因。其中上调805个差异基因，下调495个差异基因。与26个m6A系统基因进行交集，获得2个m6A基因（ZC3H13, IGFBP2）。通过分子对接发现化合物Q-1与ZC3H13有强烈的结合（total score > 7），与IGFBP2有较好的结合（total score > 5）。化合物Q-1与ZC3H13形成4个氢键（天冬氨酸1054，精氨酸999，谷氨酸1057，谷氨酰胺99），与IGFBP2形成2个（精氨酸201，亮氨酸217）。ZC3H13，IGFBP2可能通过m6A修饰调节生物代谢，为RA诊疗的靶点。化合物Q-1与ZC3H13，IGFBP2有较好的结合。

The intervention of rheumatoid arthritis gene and compound Q-1 screening based on transcriptomics combined with N6-Methyladenosine (m6A) was investigated. A collagen-induced arthritis model was replicated in rats, and the levels of interleukin1β（IL-1β), interleukin 6(IL-6), and tumour necrosis factor-alpha(TNF-α) in the serum of each group of rats were detected. Transcriptome sequencing analysis was performed on the differential genes in ankle joint tissue, and signal pathway analysis of differential genes was conducted. Intersection analysis between RA differentially expressed genes and 26 m6A system genes was performed, receiveroperating characteristic curve (ROC) analysis was carried out on zinc finger CCCH domain-containing protein 13(ZC3H13) and insulin-like growth factor binding protein 2 (IGFBP2), and molecular docking was used to analyze the binding of compound Q-1 to ZC3H13 and IGFBP2. The levels of TNF-α, IL-6, and IL-1β in the serum of the model group rats were found to be significantly increased compared to the normal control group (P <0.01). A total of 1 300 differentially expressed genes were identified in the model group compared to the normal control group, of which 805 differentially expressed genes were upregulated and 495 differentially expressed genes were downregulated. Intersection with 26 m6A system genes resulted in the obtaining of 2 m6A genes (ZC3H13, IGFBP2). Through molecular docking, it was found that compound Q-1 has strong binding to ZC3H13 (total score > 7) and good binding to IGFBP2 (total score > 5). Compound Q-1 forms four hydrogen bonds (Asp1054, Arg999, Glu1057, Gln99) with ZC3H13 and two hydrogen bonds(Arg201, Leu217) with IGFBP2. ZC3H13 and IGFBP2 may be involved in the regulation of biological metabolism through m6A modification and serve as targets for the diagnosis and treatment of RA. Compound Q-1 was found to have a good binding affinity with ZC3H13 and IGFBP2.