Pharmacodynamic material basis and anti-inflammatory mechanism of Chrysanthemum morifolium cv. Fubaiju based on UPLC-Q-TOF-MS/MS combined with network pharmacology.
10.19540/j.cnki.cjcmm.20220401.201
- Author:
Shi-Qin WANG
1
;
Dan LIU
1
;
Xiao-Chuan YE
1
;
Qian-Qian ZHU
1
;
Dan-Dan ZHANG
1
;
Bo WANG
2
;
Jing NIE
3
Author Information
1. Hubei Key Laboratory of Resource Science and Chemistry in Chinese Medicine, Pharmacy Faculty, Hubei University of Chinese Medicine Wuhan 430065, China.
2. NMPA Key Laboratory of Quality Control of Chinese Medicine, Hubei Engineering Research Center for Drug Quality Control,Hubei Institute for Drug Control Wuhan 430075, China.
3. Hubei Center for ADR Monitoring Wuhan 430071, China.
- Publication Type:Journal Article
- Keywords:
Chrysanthemum morifolium cv.Fubaiju;
UPLC-Q-TOF-MS/MS;
chemical component;
molecular docking;
network pharmacology;
pharmacodynamic materials basis;
serum pharmacochemistry
- MeSH:
Animals;
Anti-Inflammatory Agents/pharmacology*;
Chrysanthemum;
Drugs, Chinese Herbal/chemistry*;
Molecular Docking Simulation;
Network Pharmacology;
Rats;
Tandem Mass Spectrometry/methods*;
Water
- From:
China Journal of Chinese Materia Medica
2022;47(15):4190-4201
- CountryChina
- Language:Chinese
-
Abstract:
The chemical components in rats after oral administration of the water extract of Chrysanthemum morifolium cv. Fubaiju(CMF) were analyzed by UPLC-Q-TOF-MS/MS technique. Forty-four compounds were identified from the water extract of CMF and 11 components were identified from the rat serum. A total of 264 potential anti-inflammatory targets were identified by network pharmacology based on serum components. The "component-target" network and protein-protein interaction(PPI) network were constructed, and GO function enrichment and KEGG pathway enrichment analyses were performed. The molecular docking was carried out to validate the results of network pharmacology. The results showed that CMF might act on AKT1, TNF, TP53, IL6, INS, and other core targets through apigenin, luteolin, acacetin, diosmetin, 3,4-O-dicaffeoylquinic acid, and other active components, and exert anti-inflammatory effects by regulating PI3 K-AKT signaling pathway, FoxO signaling pathway, cAMP signaling pathway, Ras signaling pathway, and other pathways. The pharmacodynamic materials basis of CMF was identified by UPLC-Q-TOF-MS/MS technology, and the core anti-inflammatory targets and the underlying mechanism of action were analyzed by network pharmacology and molecular docking, which provided a reference for comprehensively clarifying the pharmacodynamic materials basis and quality control of CMF.
