PMID- 34581093
OWN - NLM
STAT- MEDLINE
DCOM- 20210929
LR  - 20210929
IS  - 1001-5302 (Print)
IS  - 1001-5302 (Linking)
VI  - 46
IP  - 18
DP  - 2021 Sep
TI  - [Molecular mechanism of Fagopyri Dibotryis Rhizoma in treatment of acute lung 
      injury based on network pharmacology and in vitro experiments].
PG  - 4816-4823
LID - 10.19540/j.cnki.cjcmm.20210524.401 [doi]
AB  - The present study explored the mechanism of Fagopyri Dibotryis Rhizoma(FDR) and 
      its main active components in the treatment of acute lung injury(ALI) based on 
      the network pharmacology and the in vitro experiments. The main active components 
      of FDR were obtained from the TCMSP database and screened by oral bioavailability 
      and drug-likeness. The related target proteins of FDR were retrieved from the 
      PubChem database, and the target genes related to ALI were screened out from the 
      GeneCards database. A protein-protein interaction(PPI) network of compound target 
      proteins and ALI target genes was constructed using STRING 11.0. Ingenuity 
      Pathway Analysis(IPA) platform was used to analyze the common pathways of the 
      potential compound target proteins of FDR and ALI target genes, thereby 
      predicting the key targets and potential signaling pathways of FDR for the 
      treatment of ALI. Finally, the potential pathways and key targets were verified 
      by the in vitro experiments of lipopolysaccharide-induced RAW264.7 cells 
      intervened by epicatechin(EC), the active component of FDR. The results of 
      network pharmacology showed that 15 potential active components such as EC, 
      procyanidin B1, and luteolin presumedly functioned in the treatment of ALI 
      through nuclear transcription factor-kappaB(NF-kappaB) signaling pathway, transforming 
      growth factor-beta(TGF-beta) signaling pathway, and adenosine 
      5'-monophosphate(AMP)-activated protein kinase(AMPK) signaling pathway through 
      key targets, such as RELA(P65). The results of in vitro experiments showed that 
      25 mumol.L~(-1) EC had no toxicity to cells and could inhibit the expression of 
      the p65-phosphorylated protein in the NF-kappaB signaling pathway to down-regulate 
      the expression of downstream inflammatory cytokines, including tumor necrosis 
      factor-alpha(TNF-alpha), IL-1beta and nitric oxide(NO), and up-regulate the expression of 
      IL-10. These results suggested that the therapeutic efficacy of FDR on ALI was 
      achieved by inhibiting the phosphorylation of p65 protein in the NF-kappaB signaling 
      pathway and down-regulating the level of proinflammatory cytokines downstream of 
      the signaling pathways.
FAU - Geng, Qi
AU  - Geng Q
AD  - College of Chemical & Biology Engineering, Yichun University Yichun 336000, China 
      Institute of Basic Research in Clinical Medicine, China Academy of Chinese 
      Medical Sciences Beijing 100700, China.
FAU - Liu, Bin
AU  - Liu B
AD  - Institute of Basic Research in Clinical Medicine, China Academy of Chinese 
      Medical Sciences Beijing 100700, China.
FAU - Zhao, Peng-Cheng
AU  - Zhao PC
AD  - School of Life Sciences, Northwestern Polytechnical University Xi'an 710000, 
      China.
FAU - Xiong, Yi-Bai
AU  - Xiong YB
AD  - Institute of Basic Research in Clinical Medicine, China Academy of Chinese 
      Medical Sciences Beijing 100700, China.
FAU - Li, Li
AU  - Li L
AD  - Institute of Basic Research in Clinical Medicine, China Academy of Chinese 
      Medical Sciences Beijing 100700, China.
FAU - Yi, Jian-Feng
AU  - Yi JF
AD  - College of Chemical & Biology Engineering, Yichun University Yichun 336000, 
      China.
FAU - Lyu, Cheng
AU  - Lyu C
AD  - Institute of Basic Research in Clinical Medicine, China Academy of Chinese 
      Medical Sciences Beijing 100700, China.
LA  - chi
PT  - Journal Article
PL  - China
TA  - Zhongguo Zhong Yao Za Zhi
JT  - Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese 
      materia medica
JID - 8913656
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
SB  - IM
MH  - *Acute Lung Injury/drug therapy/genetics
MH  - Lipopolysaccharides
MH  - NF-kappa B/genetics/metabolism
MH  - Rhizome
MH  - Signal Transduction
OTO - NOTNLM
OT  - Fagopyri Dibotryis Rhizoma
OT  - acute lung injury
OT  - molecular mechanism
OT  - network pharmacology
EDAT- 2021/09/29 06:00
MHDA- 2021/09/30 06:00
CRDT- 2021/09/28 07:04
PHST- 2021/09/28 07:04 [entrez]
PHST- 2021/09/29 06:00 [pubmed]
PHST- 2021/09/30 06:00 [medline]
AID - 10.19540/j.cnki.cjcmm.20210524.401 [doi]
PST - ppublish
SO  - Zhongguo Zhong Yao Za Zhi. 2021 Sep;46(18):4816-4823. doi: 
      10.19540/j.cnki.cjcmm.20210524.401.