大麻二酚（CBD），从大麻中提取，具有抗癌、抗炎、镇痛作用。然而，其治疗效果和缓解口腔粘膜炎（OM）的机制仍不清楚。探讨CBD对小鼠OM和人口腔角质形成细胞（HOK）细胞的影响。实验研究。中药系统药理学数据库利用GeneCard、DisGeNET和Gene Expression Omnibus分析平台等数据库对OM药物进行治疗靶点基因筛选。 Cytoscape 软件用于构建连接组件、靶点和疾病的网络。 STRING 数据库促进了目标间作用关系的分析，并且对目标基因进行了京都基因和基因组百科全书途径富集分析。血清炎症相关因子的发生、苏木精和伊红染色以及免疫组织化学用于评估 OM 损伤。评估不同处理下HOK细胞的细胞增殖、迁移、细胞焦亡和凋亡。通过蛋白质印迹和实时定量聚合酶链反应分析阐明了分子机制。总共确定了 49 个重叠基因作为潜在靶标，其中 NF-κB1、PIK3R1、NF-κBIA 和 AKT1 被认为是其中的枢纽基因。此外，PI3K/Akt/NF-κB 和 IL-17 信号通路也被确定为相关的。我们的体内实验表明，CBD显着降低了病变面积的比例，减轻了口腔粘膜组织病变，下调了NLRP3、P65、AKT和PI3K等基因和蛋白质的表达水平。体外实验表明，CBD 通过抑制 PI3K/Akt/NF-κB 信号通路和细胞焦亡，增强 HOK 细胞增殖和迁移并减少细胞凋亡。我们的研究结果提出了一种控制 OM 的新机制，其中 CBD 抑制 PI3K/Akt/ NF-κB 信号通路和细胞焦亡，从而减轻 OM 症状。

Cannabidiol (CBD), extracted from Cannabis sativa, has anticancer, anti-inflammation, and analgesic effects. Nevertheless, its therapeutic effect and the mechanism by which it alleviates oral mucositis (OM) remain unclear.To explore the impact of CBD on OM in mice and on human oral keratinocyte (HOK) cells.Expiremental study.The Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform, GeneCard, DisGeNET, and Gene Expression Omnibus databases were used to conduct therapeutic target gene screening for drugs against OM. Cytoscape software was used to build networks linking components, targets, and diseases. The STRING database facilitated analysis of intertarget action relationships, and the target genes were analyzed for Kyoto Encyclopedia of Genes and Genomes pathway enrichment. Occurrence of serum inflammation-related factors, hematoxylin and eosin staining, and immunohistochemistry were used to assess OM injury. Cell proliferation, migration, pyroptosis, and apoptosis of HOK cells under different treatments were assessed. Molecular mechanisms were elucidated through western blot and quantitative real-time polymerase chain reaction analyses.A total of 49 overlapping genes were pinpointed as potential targets, with NF-κB1, PIK3R1, NF-κBIA, and AKT1 being recognized as hub genes among them. Additionally, the PI3K/Akt/NF-κB and interleukin-17 signaling pathways were identified as relevant. Our in vivo experiments showed that CBD significantly reduced the proportion of lesion area, mitigated oral mucosal tissue lesions, and downregulated the expression levels of genes and levels of proteins, including NLRP3, P65, AKT, and PI3K. In vitro experiments indicated that CBD enhanced HOK cell proliferation and migration and reduced apoptosis through inhibition of the PI3K/Akt/NF-κB signaling pathway and pyroptosis.Our findings suggest a novel mechanism for controlling OM, in which CBD suppresses the PI3K/Akt/NF-κB signaling pathway and pyroptosis, thereby mitigating OM symptoms.