| 基于网络药理学解析舒肝方调控肝癌肠道菌群机制 |
| 投稿时间：2025-04-28 修订日期：2025-05-14 点此下载全文 |
| 引用本文：黄依婷,磨宁芳,赵嘉欣,韩秀秀,夏猛.基于网络药理学解析舒肝方调控肝癌肠道菌群机制[J].医学研究杂志,2025,54(10):32-39 |
| DOI：
10.11969/j.issn.1673-548X.2025.10.007 |
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| 基金项目:国家自然科学基金资助项目(82460921)；广西科技计划项目(桂科AB23026137)；第三批广西中医药大学“岐黄工程“高层次人才团队培育项目(202401) |
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| 中文摘要:目的 运用网络药理学解析舒肝方调控肝癌肠道菌群失调的分子机制。方法 借助TCMSP、BATMAN-TCM数据库筛选舒肝方活性成分及靶点,结合GeneCards、OMIM数据库提取肝癌与肠道菌群相关靶点,用韦恩图确定药物-疾病交集靶点。对交集靶点进行京都基因与基因组百科全书(Kyoto Encyclopedia of Genes and Genomes,KEGG)与基因本体论(Gene Ontology,GO)富集分析,采用分子对接技术验证槲皮素、堪非醇等关键成分与TP53、STAT3等核心靶点的结合活性,并通过生存分析评估靶点与肝癌预后的相关性。结果 KEGG富集分析结果显示,舒肝方主要富集于癌症通路等；GO富集分析结果显示,舒肝方参与调控细胞凋亡等过程。分子对接结果显示,关键成分与核心靶点结合稳定；生存分析结果显示,肿瘤蛋白p53基因(tumor protein p53 gene,TP53)高表达能够缩短肝癌患者的总生存期,信号转导及转录激活因子3(signal transducer and activator of transcription 3,STAT3)高表达则延长肝癌患者的生存期。结论 舒肝方或可上调STAT3、抑制TP53表达,调控相关信号通路,改善肝癌肠道菌群结构,抑制肝癌细胞增殖与转移。 |
| 中文关键词:舒肝方 肝癌 肠道菌群 网络药理学 分子对接 基因组学验证 |
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| Mechanism Elucidation of Shugan Formula Regulates Intestinal Flora in Liver Cancer Based on Network Pharmacology. |
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| Abstract:Objective To elucidate the molecular mechanism of shugan formula in regulating intestinal flora in liver cancer using network pharmacology. Methods The active components and targets of shugan formula were screened using the TCMSP and BATMAN-TCM databases. Targets associated with liver cancer and intestinal flora were extracted from the GeneCards and OMIM databases. The intersection targets between the drug and disease were identified using a Venn diagram. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analysis were performed on the intersection targets. Molecular docking technology was employed to validate the binding activities of key components, such as quercetin, kaempferol, with core targets, including TP53 and STAT3. The correlation between targets and the prognosis of liver cancer was assessed through survival analysis. Results KEGG enrichment analysis indicated that shugan formula was primarily enriched in pathways such as cancer pathways. GO enrichment analysis suggested its involvement in regulating processes like apoptosis. Molecular docking demonstrated stable binding between key components and core targets. Survival analysis revealed that high expression of tumor protein p53gene (TP53) shortened the overall survival of liver cancer patients, whereas high expression of signal transducer and activator of transcription 3 (STAT3) prolonged survival. Conclusion Shugan formula may upregulate STAT3 expression, inhibit TP53 expression, modulate relevant signaling pathways, improve the structure of intestinal flora in liver cancer, and thereby inhibit the proliferation and metastasis of liver cancer cells. |
| keywords:Shugan formula Liver cancer Intestinal flora Network pharmacology Molecular docking Genomic validation |
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