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Combinatorial Chemistry & High Throughput Screening

Editor-in-Chief

ISSN (Print): 1386-2073
ISSN (Online): 1875-5402

Research Article

Investigating the Mechanism of Shengmaiyin (Codonopsis pilosula) in the Treatment of Heart Failure Based on Network Pharmacology

Author(s): Mo Kan*, Jifeng Wang, Sitong Ming, Xin Sui, Zhuang Zhang, Qing Yang, Xiaoran Liu, Jianan Lin, Yanhong Zhang, Qihang Pang, Yaxin Liu, Zhen Li, Na Li and Zhe Lin

Volume 25, Issue 13, 2022

Published on: 14 April, 2022

Page: [2191 - 2202] Pages: 12

DOI: 10.2174/1386207325666220221093415

Price: $65

Abstract

Background and Objective: To explore the molecular mechanism by which Shengmaiyin (Codonopsis pilosula) (SMY) improves isoproterenol (ISO)-induced heart failure (HF) in rats via a traditional Chinese medicine (TCM) integrated pharmacology research platform, The Chinese Medicine Integrated Pharmacology Platform (TCMIP V2.0).

Method: The chemical constituents and drug targets of SMY medicines were identified through TCMIP, and HF disease target information was collected. A prescription Chinese medicinecomponent- core target network was constructed through the TCM network mining module, and biological process and pathway enrichment analyses of core targets were conducted. In vivo experiments in rats were performed to verify the pathway targets. Hematoxylin and eosin staining was used to observe myocardial tissue morphology. ELISA kits were used to detect cAMP content, and Western blotting was used to detect the expression levels of signaling pathway-related proteins.

Results: The TCMIP analysis indicated that SMY treatment of HF activates the GS-β-adrenergic receptor (βAR)-cAMP-protein kinase A (PKA) signaling pathway. The in vivo experimental results confirmed this finding. High-dose SMY significantly improved the morphology of ISO-injured myocardium. The levels of G-protein-coupled receptor (GPCR), adenylate cyclase (AC), βAR, and PKA proteins in myocardial tissue were significantly increased in the SMY group. In addition, the content of cAMP in myocardial tissue was increased, and the content of cAMP in serum was decreased.

Conclusion: Based on the analysis of TCMIP, SMY treatment of HF may activate the GS-βARcAMP- PKA signaling pathway. The findings provide a theoretical basis for further research on the anti-HF mechanism of SMY.

Keywords: Myocardial hypertrophy, isoproterenol hydrochloride (ISO), shengmaiyin (SMY), network pharmacology, TCMIP V2.0, GS-βAR-cAMP-PKA signaling pathway.

Graphical Abstract

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