PMID- 37986298
OWN - NLM
STAT- MEDLINE
DCOM- 20231122
LR  - 20231129
IS  - 1536-5964 (Electronic)
IS  - 0025-7974 (Print)
IS  - 0025-7974 (Linking)
VI  - 102
IP  - 46
DP  - 2023 Nov 17
TI  - Mechanism of action of Huangbaichen Sanwei formulation in treating T2DM based on 
      network pharmacology and molecular docking.
PG  - e36146
LID - 10.1097/MD.0000000000036146 [doi]
LID - e36146
AB  - Huangbaichen Sanwei formulation (HBCS) has been reported to have a good 
      hypoglycemic effect, but its pharmacological mechanism of action remains unclear. 
      We used network pharmacology and molecular docking to explore the potential 
      mechanism of action of HBCS against type-2 diabetes mellitus (T2DM). Fifty-five 
      active components from HBCS interfered with T2DM. Twenty-five core targets, such 
      as AKT1, INS, INSR, MAPK1 were identified. Enrichment analyses showed that HBCS 
      was involved mainly including insulin receptor signaling pathway, extracellular 
      region, and insulin-like growth factor receptor binding and other biological 
      processes; common targets had roles in treating T2DM by regulating diabetic 
      cardiomyopathy and insulin resistance. Molecular docking verified that components 
      combined with core targets. HBCS play a part in treating T2DM through multiple 
      components and targets at the molecular level, which lays a theoretical 
      foundation for research using HBCS to treat T2DM. The components, predicted 
      targets, and T2DM targets of HBCS were searched through databases, and common 
      targets were determined. Further screening of the core targets was conducted 
      through the establishment of a protein -protein interaction network. The core 
      targets were analyzed by Gene Ontology (GO) annotation utilizing the DAVID 
      platform. And the enrichment of signaling pathways was explored by employing the 
      Kyoto Encyclopedia of Genes and Genomes (KEGG) database. Cytoscape 3.9.1 was 
      employed to construct a "TCM-components-core target-pathway" network. Autodock 
      Vina was used to dock molecules to compare the binding activity of active 
      molecules with targets.
CI  - Copyright (c) 2023 the Author(s). Published by Wolters Kluwer Health, Inc.
FAU - Li, Chunnan
AU  - Li C
AUID- ORCID: 0000-0002-4212-0428
AD  - Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, 
      China.
FAU - Shen, Jiaming
AU  - Shen J
AD  - Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, 
      China.
FAU - Jing, Xiaolong
AU  - Jing X
AD  - College of pharmacy, Nanjing University of Chinese Medicine, Nanjing, China.
FAU - Zhang, Kaiyue
AU  - Zhang K
AD  - Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, 
      China.
FAU - Liu, Lu
AU  - Liu L
AD  - Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, 
      China.
FAU - Wang, Yuelong
AU  - Wang Y
AD  - Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, 
      China.
FAU - Zhang, Hui
AU  - Zhang H
AD  - Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, 
      China.
FAU - Sun, Jiaming
AU  - Sun J
AD  - Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, 
      China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Medicine (Baltimore)
JT  - Medicine
JID - 2985248R
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Drugs, Chinese Herbal)
SB  - IM
MH  - Humans
MH  - Molecular Docking Simulation
MH  - Network Pharmacology
MH  - *Diabetes Mellitus, Type 2/drug therapy
MH  - Protein Interaction Maps
MH  - Hypoglycemic Agents/pharmacology/therapeutic use
MH  - *Drugs, Chinese Herbal/pharmacology/therapeutic use
MH  - Medicine, Chinese Traditional
PMC - PMC10659618
COIS- The authors declare no conflict of interest, financial or otherwise.
EDAT- 2023/11/21 06:42
MHDA- 2023/11/22 06:43
PMCR- 2023/11/17
CRDT- 2023/11/21 04:50
PHST- 2023/11/22 06:43 [medline]
PHST- 2023/11/21 06:42 [pubmed]
PHST- 2023/11/21 04:50 [entrez]
PHST- 2023/11/17 00:00 [pmc-release]
AID - 00005792-202311170-00022 [pii]
AID - 10.1097/MD.0000000000036146 [doi]
PST - ppublish
SO  - Medicine (Baltimore). 2023 Nov 17;102(46):e36146. doi: 
      10.1097/MD.0000000000036146.