ArticlePharmaceuticals (Basel, Switzerland)2024
Exploring the Mechanism of Salvianolic Acid B against Myocardial Ischemia-Reperfusion Injury Based on Network Pharmacology.
Article in Pharmaceuticals (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 9 citations in OpenAlex.
- Hierarchical Au-Pt Nanostructured Film-Enabled Electrochemical Sensor for Highly-Sensitive Determination of Salvianolic Acid B.Biosensors · 2026Article
- Shionone attenuates endoplasmic reticulum stress-associated ferroptosis in cardiomyocytes by reducing LCN2 and regulating PI3K/Akt signaling.Journal of bioenergetics and biomembranes · 2026Article
- Myocardial ischemia-reperfusion injury after acute myocardial infarction: spatiotemporal mechanisms and endotype-matched multi-target modulation by compounds from traditional Chinese medicine.Frontiers in cardiovascular medicine · 2026Review
- The Traditional Chinese Medicine Compound Hezi Qingyou Formula Controls the MAPK Signaling Pathway for Alleviating Gastric Ulcer Induced by Acetic Acid in Rats.Journal of immunology research · 2026Article
- Exploring the Protective Effect and Potential Mechanism of Acutumidine on Myocardial Ischemia based on "Compound-Target-Pathway" Network.Combinatorial chemistry & high throughput screening · 2026Article
- [Salvianolic acid B promotes mitochondrial homeostasis and improves cardiac function in mice with ischemia-reperfusion injury by inhibiting Sirt1 protein degradation].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Review
- Salvianolic acid B: a promising cardioprotective agent.Frontiers in immunology · 2025Review
- Application of network pharmacology in traditional Chinese medicine for the treatment of cardiac diseases.Frontiers in pharmacology · 2025Review
- Exploring the Mechanism of Fufang Danshen Tablet against Atherosclerosis by Network Pharmacology and Experimental Validation.Pharmaceuticals (Basel, Switzerland) · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
This study aimed to explore the mechanisms through which salvianolic acid B (Sal-B) exerts its effects during myocardial ischemia-reperfusion injury (MI/RI), aiming to demonstrate the potential pharmacological characteristics of Sal-B in the management of coronary heart disease. First, Sal-B-related targets and MI/RI-related genes were compiled from public databases. Subsequent functional enrichment analyses using the protein-protein interaction (PPI) network, gene ontology (GO), and the Kyoto Encyclopedia of Genes and Genomes (KEGG) predicted the core targets and approaches by which Sal-B counters MI/RI. Second, a Sal-B-treated MI/RI mouse model and oxygen-glucose deprivation/reoxygenation (OGD/R) H9C2 cell model were selected to verify the main targets of the network pharmacological prediction. An intersectional analysis between Sal-B and MI/RI targets identified 69 common targets, with a PPI network analysis highlighting caspase-3, c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (p38) as central targets. GO and KEGG enrichment analyses indicated remarkable enrichment of the apoptosis pathway among these targets, suggesting their utility in experimental studies in vivo. Experimental results demonstrated that Sal-B treatment not only mitigated myocardial infarction size following MI/RI injury in mice but also modulated the expression of key apoptotic regulators, including Bcl-2-Associated X (Bax), caspase-3, JNK, and p38, alongside enhancing the B-cell lymphoma-2 (Bcl-2) expression, thereby inhibiting myocardial tissue apoptosis. This study leveraged an integrative network pharmacology approach to predict Sal-B's potential targets in MI/RI treatment and verified the involvement of key target proteins within the predicted signaling pathways through both in vivo and in vitro experiments, offering a comprehensive insight into Sal-B's pharmacological mechanism in MI/RI management.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.