The First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Department of Urology, Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu Province Hospital of Chinese Medicine, Nanjing, 210004, China.
Comb Chem High Throughput Screen. 2024;27(11):1661-1675. doi: 10.2174/0113862073294990240122140121.
Emodin, a compound derived from rhubarb and various traditional Chinese medicines, exhibits a range of pharmacological actions, including antiinflammatory, antiviral, and anticancer properties. Nevertheless, its pharmacological impact on bladder cancer (BLCA) and the underlying mechanism are still unclear. This research aimed to analyze the pharmacological mechanisms of Emodin against BLCA using network pharmacology analysis and experimental verification.
Initially, network pharmacology was employed to identify core targets and associated pathways affected by Emodin in bladder cancer. Subsequently, the expression of key targets in normal bladder tissues and BLCA tissues was assessed by searching the GEPIA and HPA databases. The binding energy between Emodin and key targets was predicted using molecular docking. Furthermore, experiments were carried out to confirm the predictions made with network pharmacology.
Our analysis identified 148 common genes targeted by Emodin and BLCA, with the top ten target genes including , and . Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses indicated a significant correlation between Emodin and the PI3KAKT pathway in the context of BLCA. Molecular docking investigations revealed a strong affinity between Emodin and critical target proteins. experiments demonstrated that Emodin inhibits T24 proliferation, migration, and invasion while inducing cell apoptosis. The findings also indicated that Emodin reduces both PI3K and AKT protein and mRNA expression, suggesting that Emodin may mitigate BLCA by modulating the PI3K-AKT signaling pathway.
This study integrates network pharmacology with experimentation to elucidate the potential mechanisms underlying the action of Emodin against BLCA. The results of this research enhance our understanding of the pharmacological mechanisms by which Emodin may be employed in treating BLCA.
大黄素是一种从大黄和各种中药中提取的化合物，具有多种药理作用，包括抗炎、抗病毒和抗癌作用。然而，其在膀胱癌（BLCA）中的药理作用及其机制尚不清楚。本研究旨在通过网络药理学分析和实验验证，分析大黄素对 BLCA 的药理作用机制。
首先，采用网络药理学方法鉴定大黄素对膀胱癌影响的核心靶点和相关通路。然后，通过搜索 GEPIA 和 HPA 数据库，评估关键靶点在正常膀胱组织和 BLCA 组织中的表达。利用分子对接预测大黄素与关键靶点的结合能。此外，进行实验以验证网络药理学的预测。
我们的分析确定了 148 个大黄素和 BLCA 共同作用的靶基因，其中排名前十的靶基因包括、和。基因本体论（GO）和京都基因与基因组百科全书（KEGG）通路富集分析表明，在 BLCA 背景下，大黄素与 PI3K-AKT 通路之间存在显著相关性。分子对接研究表明，大黄素与关键靶蛋白具有很强的亲和力。实验表明，大黄素抑制 T24 增殖、迁移和侵袭，同时诱导细胞凋亡。研究结果还表明，大黄素降低了 PI3K 和 AKT 蛋白和 mRNA 的表达，提示大黄素可能通过调节 PI3K-AKT 信号通路减轻 BLCA。
本研究将网络药理学与实验相结合，阐明了大黄素对 BLCA 作用的潜在机制。该研究结果提高了我们对大黄素治疗 BLCA 的药理机制的理解。
