PMID- 33149752
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220418
IS  - 1741-427X (Print)
IS  - 1741-4288 (Electronic)
IS  - 1741-427X (Linking)
VI  - 2020
DP  - 2020
TI  - Potential Molecular Mechanisms of Plantain in the Treatment of Gout and 
      Hyperuricemia Based on Network Pharmacology.
PG  - 3023127
LID - 10.1155/2020/3023127 [doi]
LID - 3023127
AB  - BACKGROUND: The incidence of gout and hyperuricemia is increasing year by year in 
      the world. Plantain is a traditional natural medicine commonly used in the 
      treatment of gout and hyperuricemia, but the molecular mechanism of its active 
      compounds is still unclear. Based on network pharmacology, this article predicts 
      the targets and pathways of effective components of plantain for gout and 
      hyperuricemia and provides effective reference for clinical medication. METHOD: 
      Traditional Chinese medicine systems pharmacology database and analysis platform 
      (TCMSP) and SymMap databases were used to screen out the active compounds and 
      their targets in plantain. GeneCards, Therapeutic Target Database (TTD), and 
      Online Mendelian Inheritance in Man (OMIM) databases were used to find the 
      targets corresponding to gout and hyperuricemia. Venn diagram was used to obtain 
      the intersection targets of plantain and diseases. The interaction network of the 
      plantain active compounds-targets-pathways-diseases was constructed by using 
      Cytoscape 3.7.2 software. Finally, Gene Ontology (GO) and Kyoto Encyclopedia of 
      Genes and Genomes (KEGG) enrichment analyses were carried out. RESULT: Seven 
      active compounds were identified by network pharmacological analysis, including 
      dinatin, baicalein, baicalin, sitosterol, 6-OH-luteolin, stigmasterol, and 
      luteolin. Plantain plays a role in gout and hyperuricemia diseases by regulating 
      various biological processes, cellular components, and molecular functions. The 
      core targets of plantain for treating gout are MAPK1, RELA, TNF, NFKBIA, and 
      IFNG, and the key pathways are pathways in cancer, hypoxia-inducible factor-1 
      (HIF-1) signaling pathway, interleukin (IL)-17 signaling pathway, Chagas disease 
      (American trypanosomiasis), and relaxin signaling pathway. The core targets of 
      plantain for hyperuricemia are RELA, MAPK1, NFKBIA, CASP3, CASP8, and TNF, and 
      the main pathways are pathways in cancer, apoptosis, hepatitis B, IL-17 signaling 
      pathway, and toxoplasmosis. CONCLUSION: This study explored the related targets 
      and mechanisms of plantain for the treatment of gout and hyperuricemia from the 
      perspective of network pharmacological analysis, reflecting the characteristics 
      of multiple components, multiple targets, and multiple pathways, and it provides 
      a good theoretical basis for the clinical application of plantain.
CI  - Copyright (c) 2020 Pei Liu et al.
FAU - Liu, Pei
AU  - Liu P
AUID- ORCID: 0000-0002-9972-3449
AD  - College of Traditional Chinese Medicine, Jinan University, Guangzhou 510632, 
      China.
FAU - Xu, Huachong
AU  - Xu H
AUID- ORCID: 0000-0003-4046-7599
AD  - College of Traditional Chinese Medicine, Jinan University, Guangzhou 510632, 
      China.
FAU - Shi, Yucong
AU  - Shi Y
AUID- ORCID: 0000-0002-8075-8078
AD  - College of Traditional Chinese Medicine, Jinan University, Guangzhou 510632, 
      China.
FAU - Deng, Li
AU  - Deng L
AUID- ORCID: 0000-0002-1522-4184
AD  - College of Traditional Chinese Medicine, Jinan University, Guangzhou 510632, 
      China.
FAU - Chen, Xiaoyin
AU  - Chen X
AUID- ORCID: 0000-0001-5109-4287
AD  - College of Traditional Chinese Medicine, Jinan University, Guangzhou 510632, 
      China.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20201022
PL  - United States
TA  - Evid Based Complement Alternat Med
JT  - Evidence-based complementary and alternative medicine : eCAM
JID - 101215021
PMC - PMC7603577
COIS- The authors declare that they have no conflicts of interest.
EDAT- 2020/11/06 06:00
MHDA- 2020/11/06 06:01
PMCR- 2020/10/22
CRDT- 2020/11/05 06:07
PHST- 2020/03/21 00:00 [received]
PHST- 2020/07/13 00:00 [revised]
PHST- 2020/08/04 00:00 [accepted]
PHST- 2020/11/05 06:07 [entrez]
PHST- 2020/11/06 06:00 [pubmed]
PHST- 2020/11/06 06:01 [medline]
PHST- 2020/10/22 00:00 [pmc-release]
AID - 10.1155/2020/3023127 [doi]
PST - epublish
SO  - Evid Based Complement Alternat Med. 2020 Oct 22;2020:3023127. doi: 
      10.1155/2020/3023127. eCollection 2020.