Kunshan Hospital of Chinese Medicine, Kunshan, 215300, PR China.
Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Zhangjiagang, 215600, PR China.
BMC Complement Med Ther. 2024 Jul 23;24(1):280. doi: 10.1186/s12906-024-04590-3.
Huangkui Lianchang Decoction (HLD) is a traditional Chinese herbal formula for treating ulcerative colitis (UC). However, its mechanism of action remains poorly understood. The Study aims to validate the therapeutic effect of HLD on UC and its mechanism by integrating network pharmacology, bioinformatics, and experimental validation.
UC targets were collected by databases and GSE19101. The active ingredients in HLD were detected by ultra-performance liquid chromatography-tandem mass spectrometry. PubChem collected targets of active ingredients. Protein-protein interaction (PPI) networks were established with UC-related targets. Gene Ontology and Kyoto Encyclopedia (KEGG) of Genes and Genomes enrichment were analyzed for the mechanism of HLD treatment of UC and validated by the signaling pathways of HLD. Effects of HLD on UC were verified using dextran sulfate sodium (DDS)-induced UC mice experiments.
A total of 1883 UC-related targets were obtained from the GSE10191 dataset, 1589 from the database, and 1313 matching HLD-related targets, for a total of 94 key targets. Combined with PPI, GO, and KEGG network analyses, the signaling pathways were enriched to obtain IL-17, Toll-like receptor, NF-κB, and tumor necrosis factor signaling pathways. In animal experiments, HLD improved the inflammatory response of UC and reduced UC-induced pro-inflammatory factors such as Tumor Necrosis Factor Alpha (TNF-α), interleukin 1β (IL-1β), and interleukin 6 (IL-6). HLD suppressed proteins TLR4, MyD88, and NF-κB expression.
This study systematically dissected the molecular mechanism of HLD for the treatment of UC using a network pharmacology approach. Further animal verification experiments revealed that HLD inhibited inflammatory responses and improved intestinal barrier function through the TLR4/MyD88/NF-κB pathway.
黄葵连肠汤（HLD）是一种治疗溃疡性结肠炎（UC）的中药方剂。然而，其作用机制仍不清楚。本研究旨在通过整合网络药理学、生物信息学和实验验证，验证 HLD 对 UC 的治疗作用及其机制。
通过数据库和 GSE19101 收集 UC 靶点。采用超高效液相色谱-串联质谱法检测 HLD 中的活性成分。从 PubChem 收集活性成分的靶点。建立 UC 相关靶点的蛋白质-蛋白质相互作用（PPI）网络。对 HLD 治疗 UC 的机制进行基因本体论和京都基因与基因组百科全书（KEGG）基因和基因组富集分析，并通过 HLD 信号通路进行验证。采用葡聚糖硫酸钠（DDS）诱导 UC 小鼠实验验证 HLD 对 UC 的作用。
从 GSE10191 数据集获得 1883 个 UC 相关靶点，从数据库获得 1589 个，与 HLD 相关靶点匹配获得 1313 个，共获得 94 个关键靶点。结合 PPI、GO 和 KEGG 网络分析，富集信号通路，获得 IL-17、Toll 样受体、NF-κB 和肿瘤坏死因子信号通路。在动物实验中，HLD 改善了 UC 的炎症反应，降低了 UC 诱导的促炎因子如肿瘤坏死因子-α（TNF-α）、白细胞介素 1β（IL-1β）和白细胞介素 6（IL-6）。HLD 抑制了 TLR4、MyD88 和 NF-κB 蛋白的表达。
本研究采用网络药理学方法系统剖析了 HLD 治疗 UC 的分子机制。进一步的动物验证实验表明，HLD 通过 TLR4/MyD88/NF-κB 通路抑制炎症反应，改善肠道屏障功能。
