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Study on the mechanism of Codonopsis Radix ameliorating H2O2-induced myocardial cell injury
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DOI   10.11656/j.issn.1673-9043.2025.06.05
Key Words   Codonopsis Radix;myocardial injury;oxidative stress;apoptosis;network pharmacology
Author NameAffiliationE-mail
DU Siqi Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China  
QI Yulin Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China  
BAI Liding Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China  
ZHOU Fengjie Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China  
WANG Ting Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China  
LI Lin Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China
State Key Laboratory of Components-based Chinese Medicine, Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China 
 
LI Yuhong Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China
State Key Laboratory of Components-based Chinese Medicine, Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China 
liyuhong@tjutcm.edu.cn 
Abstract
    [Objective] To investigate the effect and potential mechanism of Codonopsis Radix(CR) in preventing myocardial injury by network pharmacology combined with in vitro experiments.[Methods] The active ingredients and targets of CR were obtained from Traditional Chinese Medicine System Pharmacology(TCMSP) and SwissTargetPrediction databases, and the targets related to myocardial injury were obtained by using GeneCards database, and the “component-target-disease” network and protein-protein interaction(PPI) network diagram were constructed by using Cytoscape. Gene ontology(GO) analysis and kyoto Encyclopedia of Genes and Genomes(KEGG) enrichment analysis were performed on the intersection targets by using the Annotation, Visualization, and Integrated Discovery(DAVID) database, to predict CR potential targets for the treatment of myocardial injury. H9c2 cardiomyocytes stimulated by hydrogen peroxide(H2O2, 300 μmol/L) were treated with different concentrations of CR(50 and 100 μg/mL) in vitro, and the content of mitochondrial reactive oxygen species(ROS) was detected by ROS fluorescent probe. The biochemical kit was used to detect the levels of malondialdehyde(MDA) and superoxide dismutase(SOD) in cardiomyocytes. Western Blot was used to detect the expressions of apoptosis-related proteins bcl-2-associated X protein(Bax), cysteine protease-3(Caspase-3) and cytochrome C(Cytochrome C), to investigate the potential mechanism of CR in anti-myocardial injury.[Results] Network pharmacology analysis revealed 21 active ingredients and 278 potential targets of CR. There were 835 myocardial injury-related targets and 106 intersecting targets. GO and KEGG enrichment analysis showed that the protection of CR on cardiomyocyte injury mainly involved PI3K-Akt signaling pathway, chemical carcinogenesis-reactive oxygen species and apoptosis signaling pathway. The results of cell experiments showed that 50 and 100 μg/mL CR could significantly reduce the content of MDA and mitochondrial ROS in cardiomyocytes, and increase the level of SOD. Western Blot results showed that CR inhibited the expression of pro-apoptotic proteins Bax, Cytochrome C and Caspase-3.[Conclusion] CR may exert a protective effect on cardiomyocytes by inhibiting apoptosis caused by oxidative stress.

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