Liang-Ge-San Decoction Ameliorates Acute Respiratory Distress Syndrome via Suppressing p38MAPK-NF-κ B Signaling Pathway.
10.1007/s11655-024-3769-6
- Author:
Quan LI
1
;
Juan CHEN
2
;
Meng-Meng WANG
2
;
Li-Ping CAO
2
;
Wei ZHANG
2
;
Zhi-Zhou YANG
2
;
Yi REN
2
;
Jing FENG
2
;
Xiao-Qin HAN
2
;
Shi-Nan NIE
2
;
Zhao-Rui SUN
3
,
4
Author Information
1. Department of Intensive Care Unit, Suqian First Hospital, Suqian, Jiangsu Province, 223800, China.
2. Department of Emergency Medicine, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210002, China.
3. Department of Emergency Medicine, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210002, China. sunzhr84@
4. com.
- Publication Type:Journal Article
- Keywords:
Liang-Ge-San;
acute respiratory distress syndrome;
animal experiments;
molecular docking;
network pharmacology
- MeSH:
Drugs, Chinese Herbal/pharmacology*;
Respiratory Distress Syndrome/enzymology*;
p38 Mitogen-Activated Protein Kinases/metabolism*;
NF-kappa B/metabolism*;
Animals;
Signal Transduction/drug effects*;
Molecular Docking Simulation;
Humans;
Male;
Network Pharmacology;
Apoptosis/drug effects*;
Mice
- From:
Chinese journal of integrative medicine
2025;31(7):613-623
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:To explore the potential effects and mechanisms of Liang-Ge-San (LGS) for the treatment of acute respiratory distress syndrome (ARDS) through network pharmacology analysis and to verify LGS activity through biological experiments.
METHODS:The key ingredients of LGS and related targets were obtained from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform. ARDS-related targets were selected from GeneCards and DisGeNET databases. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed using the Metascape Database. Molecular docking analysis was used to confirm the binding affinity of the core compounds with key therapeutic targets. Finally, the effects of LGS on key signaling pathways and biological processes were determined by in vitro and in vivo experiments.
RESULTS:A total of LGS-related targets and 496 ARDS-related targets were obtained from the databases. Network pharmacological analysis suggested that LGS could treat ARDS based on the following information: LGS ingredients luteolin, wogonin, and baicalein may be potential candidate agents. Mitogen-activated protein kinase 14 (MAPK14), recombinant V-Rel reticuloendotheliosis viral oncogene homolog A (RELA), and tumor necrosis factor alpha (TNF-α) may be potential therapeutic targets. Reactive oxygen species metabolic process and the apoptotic signaling pathway were the main biological processes. The p38MAPK/NF-κ B signaling pathway might be the key signaling pathway activated by LGS against ARDS. Moreover, molecular docking demonstrated that luteolin, wogonin, and baicalein had a good binding affinity with MAPK14, RELA, and TNF α. In vitro experiments, LGS inhibited the expression and entry of p38 and p65 into the nucleation in human bronchial epithelial cells (HBE) cells induced by LPS, inhibited the inflammatory response and oxidative stress response, and inhibited HBE cell apoptosis (P<0.05 or P<0.01). In vivo experiments, LGS improved lung injury caused by ligation and puncture, reduced inflammatory responses, and inhibited the activation of p38MAPK and p65 (P<0.05 or P<0.01).
CONCLUSION:LGS could reduce reactive oxygen species and inflammatory cytokine production by inhibiting p38MAPK/NF-κ B signaling pathway, thus reducing apoptosis and attenuating ARDS.
