Pharmacodynamic material basis and mechanism of Fufang Yuxingcao Mixture for the treatment of heat-clearing and detoxification based on network pharmacology
10.16438/j.0513-4870.2021-0085
- VernacularTitle:基于网络药理学的复方鱼腥草合剂清热解毒药效物质基础及作用机制研究
- Author:
Yan-qi HAN
1
,
2
;
Zhi-lin CHEN
3
;
Yao-chen LIU
4
;
Jiang-ning HU
5
;
Jun XU
1
,
2
;
Hong-bing ZHANG
1
,
2
;
Jian-ting LIU
1
,
2
;
Yang ZHANG
1
,
2
;
Tie-jun ZHANG
1
,
2
;
Chang-xiao LIU
1
,
2
Author Information
1. Tianjin Key Laboratory of Quality Marker of Traditional Chinese Medicine, Tianjin 300462, China
2. State Key Laboratory of Drug Delivery and Pharmacokinetics, Tianjin Institute of Pharmaceutical Research, Tianjin 300462, China
3. Zhejiang CONBA Chinese Medicine Co., LTD., Lishui 323400, China
4. Tianjin Medical University, Tianjin 300070, China
5. Zhejiang CONBA Pharmaceutical Co., LTD., Hangzhou 310052, China
- Publication Type:Research Article
- Keywords:
Fufang Yuxingcao Mixture;
network pharmacology;
pharmacodynamic material basis;
mechanism;
heat-clearing and detoxification
- From:
Acta Pharmaceutica Sinica
2021;56(6):1653-1662
- CountryChina
- Language:Chinese
-
Abstract:
We explored the pharmacodynamic material basis and network regulatory mechanism of Fufang Yuxingcao Mixture (FYM) for the treatment of fever and inflammation. Targets of the 25 compounds in FYM were predicted according to the reverse pharmacophore method and TCMSP, UniProt database. Gene ontology (GO) function enrichment and pathway analysis of the targets was analyzed by Omicsbean software and the Kyoto Gene and Genome Encyclopedia (KEGG) database. A "compound-target-pathway-pharmacological action-effect" network was established with Cytoscape 3.6.1 software. The lipopolysaccharide (LPS)-induced RAW264.7 cell inflammation model was used to verify the anti-inflammatory effects of FYM and its 10 important components. The network pharmacology experiment showed that 25 compounds affected 97 pathways through 211 targets, of which 15 key targets [including RAC-alpha serine/threonine-protein kinase (AKT1), insulin (INS), vascular endothelial growth factor A (VEGFA), interleukin-6 (IL-6), cellular tumor antigen p53 (TP53), tumor necrosis factor (TNF), transcription factor AP-1 (JUN), caspase-3 (CASP3), matrix metalloproteinase-9 (MMP9), interleukin-8 (IL-8), prostaglandin G/H synthase 2 (PTGS2), proto-oncogene c-Fos (FOS), tyrosine-protein kinase SRC (SRC), c-Jun N-terminal kinase 1 (MAPK8), estrogen receptor 1 (ESR1)] and 46 pathways (including NF-kappa B signaling pathway, Toll-like receptor signaling pathway, MAPK signaling pathway, IL-17 signaling pathway, arachidonic acid metabolism, cAMP signaling pathway, T cell receptor signaling pathway, calcium signaling pathway, inflammatory mediator regulation of TRP channels, chemokine signaling pathway, Th1 and Th2 cell differentiation, natural killer cell mediated cytotoxicity, etc.) were related to anti-inflammatory, antipyretic, immune regulation, and analgesia. In vitro cell experiments showed that FYM and the 10 components (including isoquercitrin, luteoloside, baicalein, wogonin, wogonoside, phillyrin, forsythoside A, chlorogenic acid, isochlorogenic acid A, and sweroside) could significantly reduce the expression of nitric oxide (NO), TNF-α and IL-6 in cell supernatants, indicating that the above 10 components may be the key pharmacodynamic material basis of FYM.
