Department of Clinical Pharmacy, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing 211198, China.
Precision Medicine Laboratory, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing 211198, China.
Curr Pharm Des. 2024;30(4):278-294. doi: 10.2174/0113816128280351240112044430.
Chaiqin Qingning capsule (CQQNC) has been used to relieve pain in practice. However, the active components, pain targets, and molecular mechanisms for pain control are unclear.
To explore the active components and potential mechanisms of the analgesic effect of CQQNC through network pharmacology and experiments.
The main active components and the corresponding targets of CQQNC were screened from the TCMSP and the SwissTargetPrediction databases. Pain-related targets were selected in the OMIM, Gene- Cards, and DrugBank databases. These targets were intersected to obtain potential analgesic targets. The analgesic targets were imported into the STRING and DAVID databases for protein-protein interaction (PPI), gene ontology (GO) function enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. Cytoscape software (V3.7.1) was used to construct an active component-intersection network. Finally, the key components were docked with the core targets. The analgesic mechanism of CQQNC was verified by RAW264.7 cell experiment.
30 active CQQNC components, 617 corresponding targets, and 3,214 pain-related target genes were found. The main active components were quercetin, kaempferol, and chenodeoxycholic acid etc. The key targets were ALB, AKT1, TNF, IL6, TP53, IL1B, and SRC. CQQNC can exert an analgesic effect through PI3K-Akt, MAPK signaling pathways, etc. Molecular docking showed that these active components had good binding activities with key targets. The results of experiments showed that CQQNC could exert antiinflammatory and analgesic effects through MAPK/AKT/NF-kB signaling pathways.
CQQNC exerts pain control through inhibiting MAPK/AKT/NF-kB signaling pathways.
柴芩清宁胶囊在临床上被用于缓解疼痛。然而，其活性成分、疼痛靶点和分子机制尚不清楚。
通过网络药理学和实验方法探讨柴芩清宁胶囊的镇痛作用的活性成分和潜在机制。
从 TCMSP 和 SwissTargetPrediction 数据库中筛选柴芩清宁胶囊的主要活性成分及其相应的靶点。在 OMIM、GeneCards 和 DrugBank 数据库中选择与疼痛相关的靶点。将这些靶点进行交集，获得潜在的镇痛靶点。将镇痛靶点导入 STRING 和 DAVID 数据库进行蛋白质-蛋白质相互作用（PPI）、基因本体（GO）功能富集和京都基因与基因组百科全书（KEGG）通路富集分析。使用 Cytoscape 软件（V3.7.1）构建活性成分交集网络。最后，用关键成分对核心靶点进行对接。通过 RAW264.7 细胞实验验证柴芩清宁胶囊的镇痛机制。
发现 30 种柴芩清宁胶囊的活性成分、617 个相应靶点和 3214 个与疼痛相关的靶基因。主要活性成分为槲皮素、山奈酚、鹅去氧胆酸等。关键靶点为 ALB、AKT1、TNF、IL6、TP53、IL1B 和 SRC。柴芩清宁胶囊可以通过 PI3K-Akt、MAPK 等信号通路发挥镇痛作用。分子对接表明这些活性成分与关键靶点具有良好的结合活性。实验结果表明，柴芩清宁胶囊通过 MAPK/AKT/NF-kB 信号通路发挥抗炎和镇痛作用。
柴芩清宁胶囊通过抑制 MAPK/AKT/NF-kB 信号通路发挥镇痛作用。
