Abstract：
UNASSIGNED: 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.
UNASSIGNED: To explore the impact of CBD on OM in mice and on human oral keratinocyte (HOK) cells.
UNASSIGNED: Expiremental study.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: To explore the impact of CBD on OM in mice and on human oral keratinocyte (HOK) cells.
UNASSIGNED: Expiremental study.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
摘要：
■大麻二酚（CBD），从大麻中提取，有抗癌作用,抗炎，和镇痛作用。然而，其治疗效果及其缓解口腔黏膜炎(OM)的机制尚不清楚.
■探讨CBD对小鼠OM和人口腔角质形成细胞（HOK）细胞的影响。
■过期研究。
■中药系统药理学数据库与分析平台,GeneCard,DisGeNet,和基因表达Omnibus数据库用于进行抗OM药物的治疗靶基因筛选。Cytoscape软件用于构建连接组件的网络，目标,和疾病。STRING数据库促进了目标间行动关系的分析，并对目标基因进行了京都基因百科全书和基因组途径富集分析。血清炎症相关因子的发生,苏木精和伊红染色，和免疫组织化学用于评估OM损伤。细胞增殖，迁移,焦亡,并对不同处理条件下HOK细胞的凋亡情况进行评估。通过蛋白质印迹和定量实时聚合酶链反应分析阐明了分子机制。
■总共有49个重叠基因被确定为潜在的靶标，与NF-κB1，PIK3R1，NF-κBIA，AKT1被认为是其中的枢纽基因。此外,PI3K/Akt/NF-κB和白细胞介素-17信号通路被鉴定为相关的。我们的体内实验表明，CBD显着减少病变面积的比例，缓解口腔粘膜组织病变，下调基因表达水平和蛋白质水平，包括NLRP3，P65，AKT，PI3K体外实验表明，CBD通过抑制PI3K/Akt/NF-κB信号通路和焦凋亡，增强HOK细胞增殖和迁移，减少凋亡。
■我们的研究结果表明了一种控制OM的新机制，其中CBD抑制PI3K/Akt/NF-κB信号通路和焦亡，从而减轻OM症状。
■探讨CBD对小鼠OM和人口腔角质形成细胞（HOK）细胞的影响。
■过期研究。
■中药系统药理学数据库与分析平台,GeneCard,DisGeNet,和基因表达Omnibus数据库用于进行抗OM药物的治疗靶基因筛选。Cytoscape软件用于构建连接组件的网络，目标,和疾病。STRING数据库促进了目标间行动关系的分析，并对目标基因进行了京都基因百科全书和基因组途径富集分析。血清炎症相关因子的发生,苏木精和伊红染色，和免疫组织化学用于评估OM损伤。细胞增殖，迁移,焦亡,并对不同处理条件下HOK细胞的凋亡情况进行评估。通过蛋白质印迹和定量实时聚合酶链反应分析阐明了分子机制。
■总共有49个重叠基因被确定为潜在的靶标，与NF-κB1，PIK3R1，NF-κBIA，AKT1被认为是其中的枢纽基因。此外,PI3K/Akt/NF-κB和白细胞介素-17信号通路被鉴定为相关的。我们的体内实验表明，CBD显着减少病变面积的比例，缓解口腔粘膜组织病变，下调基因表达水平和蛋白质水平，包括NLRP3，P65，AKT，PI3K体外实验表明，CBD通过抑制PI3K/Akt/NF-κB信号通路和焦凋亡，增强HOK细胞增殖和迁移，减少凋亡。
■我们的研究结果表明了一种控制OM的新机制，其中CBD抑制PI3K/Akt/NF-κB信号通路和焦亡，从而减轻OM症状。
