IMR Press / FBL / Volume 26 / Issue 10 / DOI: 10.52586/4990
Open Access Original Research
Exploration of the active components and pharmacological mechanism of Compound Longmaining for the treatment of myocardial infarction
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1 Department of Pharmaceutics, College of Pharmacy, Shaanxi University of Chinese Medicine, 712000 Xianyang, Shaanxi, China
2 Affiliated Hospital of Shaanxi University of Chinese Medicine, 712000 Xianyang, Shaanxi, China
*Correspondence: (Xiaofei Zhang); (Changli Wang)
These authors contributed equally.
Front. Biosci. (Landmark Ed) 2021, 26(10), 813–827;
Submitted: 22 April 2021 | Revised: 10 August 2021 | Accepted: 20 August 2021 | Published: 30 October 2021
Copyright: © 2021 The Author(s). Published by BRI.
This is an open access article under the CC BY 4.0 license (

Background: Myocardial Infarction (MI) is a cardiovascular disease with a high morbidity and mortality rate. While MI is currently treated with pharmaceuticals, there is a need for new treatment options: compound Chinese medicines may have unique advantages for the treatment of MI. Methods: A combination of network pharmacology and experimental verification is used to identify the ingredients and mechanism of Compound Longmaining (CLMN) for treating MI. Network pharmacology combined with the gene expression omnibus (GEO) chip method is used to analyze the primary pathway of CLMN for treating MI, and then molecular docking is used to verify the affinity of key target proteins in the primary pathway that bind to active molecules. The major active compounds of CLMN are screened using the docking score results. The CIBERSORT algorithm is used to evaluate immune cell infiltration in MI, and high performance liquid chromatography (HPLC) is used to control the quality of the components. Finally, a mouse model is established to verify the molecular mechanism of CLMN for treating MI using hematoxlyn eosin (HE) staining and immunohistochemistry. Results: By utilizing network pharmacology combined with molecular docking, the mechanism of action of CLMN for the treatment of MI was found to possibly be related to the ingredients of puerarin, daidzein, ferulic acid, chrysin, and galangin. These molecules regulate the NF-Kappa B signaling pathway and the expression of RELA, IKBKB, NKBIA, and other targets. The CIBERSORT algorithm and ggplot2 package analysis were used to distinguish the immune cells, such as neutrophils, macrophages, and T cells, that play a key role in the development of MI. HPLC controlled the quality of the screened medicinal ingredients. An immunohistochemical analysis showed that the TNF-α and TRAF-2 expression levels in MI of the CLMN-treated mice were decreased, while IkBα was increased. HE staining showed CLMN reduced inflammation in mouse cardiomyocytes and decreased fibrosis. Conclusions: This study showed that CLMN treatment of MI is a process that involves multi-components, multi-targets and multi-pathways, and the established multi-index component content measurement of the CLMN decoction can be used for quality control of CLMN.

Network pharmacology
Compound Longmaining decoction
Myocardial infarction
Immune cell infiltration
Quality control
NF-Kappa B signaling pathway
Fig. 1.
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