ArticleDrug design, development and therapy2024
Network and Experimental Pharmacology on Mechanism of Yixintai Regulates the TMAO/PKC/NF-κB Signaling Pathway in Treating Heart Failure.
Article in Drug design, development and therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
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Who cites it
11 citing papers in PubMed.
- Traditional Chinese Medicine Intervention Based on Metabolic-Epigenetic Axis: Mechanism and Treatment Strategy of Chronic Heart Failure.Biomolecules · 2026Review
- Multi-Omics Mechanisms of Trimethylamine Oxide and Cardiovascular Disease: A Review.Reviews in cardiovascular medicine · 2026Review
- PRRs-related genes and immune landscape in heart failure and COPD.Scientific reports · 2026Article
- The gut-heart axis in heart failure: from bidirectional pathophysiological mechanisms to integrative therapeutic strategies.Frontiers in microbiology · 2026Review
- Role of Gut Microbiota in Diabetic HFpEF: Mechanisms and Therapeutic Implications.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Classification of intestinal inflammation driven by gut microbiota metabolites: a new paradigm for precision treatment of cardiovascular diseases.Frontiers in microbiology · 2026Review
- Role of Gut Microbial Metabolites in Ischemic and Non-Ischemic Heart Failure.International journal of molecular sciences · 2025Review
- Review
- The gut microbiota-inflammation-HFpEF axis: deciphering the role of gut microbiota dysregulation in the pathogenesis and management of HFpEF.Frontiers in cellular and infection microbiology · 2025Review
- Yixintai treats chronic heart failure in rats by regulating gut microbiota and bile acid.Frontiers in microbiology · 2025Article
- Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: This study aims to explore the mechanism of action of Yixintai in treating chronic ischemic heart failure by combining bioinformatics and experimental validation. Materials and Methods: Five potential drugs for treating heart failure were obtained from Yixintai (YXT) through early mass spectrometry detection. The targets of YXT for treating heart failure were obtained by a search of online databases. Gene ontology (GO) functional enrichment analysis and Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analyses were conducted on the common targets using the DAVID database. A rat heart failure model was established by ligating the anterior descending branch of the left coronary artery. A small animal color Doppler ultrasound imaging system detected cardiac function indicators. Hematoxylin-eosin (HE), Masson's, and electron microscopy were used to observe the pathological morphology of the myocardium in rats with heart failure. The network pharmacology analysis results were validated by ELISA, qPCR, and Western blotting. Results: A total of 107 effective targets were obtained by combining compound targets and eliminating duplicate values. PPI analysis showed that inflammation-related proteins (TNF and IL1B) were key targets for treating heart failure, and KEGG enrichment suggested that NF-κB signaling pathway was a key pathway for YXT treatment of heart failure. Animal model validation results indicated the following: YXT can significantly reduce the content of intestinal microbiota metabolites such as trimethylamine oxide (TMAO) and improve heart failure by improving the EF and FS values of heart ultrasound in rats and reducing the levels of serum NT-proBNP, ANP, and BNP to improve heart failure. Together, YXT can inhibit cardiac muscle hypertrophy and fibrosis in rats and improve myocardial ultrastructure and serum IL-1β, IL-6, and TNF-α levels. These effects are achieved by inhibiting the expressions of NF-κB and PKC. Conclusion: YXT regulates the TMAO/PKC/NF-κB signaling pathway in heart failure.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.