败酱草和薏苡仁 (HC) 是结直肠癌 (CRC) 临床治疗中广泛使用的药物组合，以其利尿、抗炎和消肿特性而闻名。尽管其功效已在临床环境中得到证实，但活性化合物及其在 CRC 治疗中的作用机制仍有待充分阐明。鉴定 HC 的活性、CRC 靶向成分并阐明相关作用机制。活性 HC使用数据库来识别和筛选组件。预测了每个组件的目标。 CRC相关靶标是从人类基因数据库中获得的。确定了 HC 和 CRC 之间的相互作用目标。创建了“药物-成分-目标”网络来识别所涉及的核心成分和目标。进行基因本体论（GO）和京都基因和基因组百科全书（KEGG）分析以阐明所涉及的关键途径。进行了核心靶点与关键成分之间的分子对接。体外实验验证了核心单体。鉴定出 HC 的 19 种活性成分，其中金合欢素为主要活性化合物。预测分析确定了 HC 中活性化合物的 454 个目标。与 2685 个 CRC 相关目标的交叉点映射产生了 171 个干预目标，其中包括 30 个核心目标。 GO和KEGG分析表明HC可能影响磷酸肌醇3激酶(PI3K)/Akt信号通路。分子对接显示金合欢素与 AKT1 表现出最佳的相互作用，将 PI3K、AKT 和 P53 确定为 CRC 治疗期间可能被 HC 靶向的关键基因。在体外，Acacetin 抑制 HT-29 细胞增殖和迁移，并促进细胞凋亡。 Western blotting 分析显示，p53 和 cleaved caspase-3 表达增加，p-PI3K、p-Akt 和 survivin 水平降低，这可能导致 CRC 凋亡。Acacetin 是 HC 对中的主要活性化合物，可抑制增殖和迁移通过 PI3K/Akt/p53 信号通路促进 HT-29 细胞凋亡。©作者 2024。百世登出版集团有限公司出版。保留所有权利。

Herba Patriniae and Coix seed (HC) constitute a widely utilized drug combination in the clinical management of colorectal cancer (CRC) that is known for its diuretic, anti-inflammatory, and swelling-reducing properties. Although its efficacy has been demonstrated in a clinical setting, the active compounds and their mechanisms of action in CRC treatment remain to be fully elucidated.To identify the active, CRC-targeting components of HC and to elucidate the mechanisms of action involved.Active HC components were identified and screened using databases. Targets for each component were predicted. CRC-related targets were obtained from human gene databases. Interaction targets between HC and CRC were identified. A "drug-ingredient-target" network was created to identify the core components and targets involved. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were conducted to elucidate the key pathways involved. Molecular docking between core targets and key components was executed. In vitro experiments validated core monomers.Nineteen active components of HC were identified, with acacetin as the primary active compound. The predictive analysis identified 454 targets of the active compounds in HC. Intersection mapping with 2685 CRC-related targets yielded 171 intervention targets, including 30 core targets. GO and KEGG analyses indicated that HC may influence the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. Molecular docking showed that acacetin exhibited an optimal interaction with AKT1, identifying PI3K, AKT, and P53 as key genes likely targeted by HC during CRC treatment. Acacetin inhibited HT-29 cell proliferation and migration, as well as promoted apoptosis, in vitro. Western blotting analysis revealed increased p53 and cleaved caspase-3 expression and decreased levels of p-PI3K, p-Akt, and survivin, which likely contributed to CRC apoptosis.Acacetin, the principal active compound in the HC pair, inhibited the proliferation and migration of HT-29 cells and promoted apoptosis through the PI3K/Akt/p53 signaling pathway.©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.