ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Exploring the mechanism of Cucurbitacin B against myocardial ischemia reperfusion injury based on network pharmacology and experimental validation.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Myocardial ischemia/reperfusion injury (MI/RI) is a complex state involving numerous inflammatory mediators, which significantly worsens the outcomes of patients with cardiovascular diseases. However, no standardized treatment plan for MI/RI prevails at present. Cucurbitacin B (Cb-B) is a natural bioactive substance extracted from the stem of melon flowers, and is associated with Wnt-β-Catenin, NF-κB, and PI3K/AKT signaling pathways to initiate apoptosis and inflammatory responses in various cancers. Nevertheless, its potential preventive role in MI/RI remains unclear. Here, the potential mechanism adopted by Cb-B for alleviating MI/RI was explored by network pharmacology and in vivo experiments. Firstly, network pharmacology methods, including multiple data retrieval, network construction analysis, gene ontology enrichment analysis, pathway analysis, and molecular docking, were employed to identify the target genes, signaling pathways, and potential mechanisms of Cb-B in the possible treatment of MI/RI. Simultaneously, results were validated through in vivo experiments. The results showed that the comprehensive network pharmacology identified cellular pyroptosis and apoptosis-related genes as nlrp3, caspase1, bcl-2, and caspase3. Functional enrichment analysis showed the association of these target genes with inflammatory response, positive regulation of cytokine production, and response to lipopolysaccharides in biological processes. In addition, the MI/RI rat model showed that Cb-B could alleviate myocardial injury by reducing the release of cellular pyroptosis and apoptosis-related genes. These results suggested that the mechanism of cardioprotective effects of Cb-B may be related to the regulation of PTEN/PI3K/AKT signaling pathways, which lays a foundation for further research on MI/RI treatment.
Indexed as
Identifiers
41609855What 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.