ArticleDie Naturwissenschaften2026
Bellidifolin alleviates doxorubicin-induced hepatotoxicity: a study integrating network pharmacology, molecular docking, and experimental validation.
Article in Die Naturwissenschaften, 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
8 authors.
Funding
Abstract
This study aimed to investigate the protective role of bellidifolin (BEL) in doxorubicin (DOX)-induced liver injury and explore its underlying mechanisms. Through network pharmacology, potential targets and pathways of BEL against DOX-induced liver injury were identified. Molecular docking and molecular dynamics simulation were employed to further verify the binding activity of BEL to the core targets. Mice were randomly divided into three groups: control (CON), DOX (DOX) and BEL treated group (BEL). Liver pathological changes were evaluated through HE and Masson staining, serum ALT and AST were detected using a biochemical analyzer, and predicted pathway related proteins were assessed through immunohistochemistry staining and western blot analysis. Results: BEL alleviated DOX-induced liver injury in mice, as evidenced by attenuated hepatic pathological changes and fibrosis, decreased serum levels of ALT and AST, and inhibition of hepatocyte pyroptosis. The network pharmacology analysis revealed that the key targets of BEL in treating DOX-induced liver injury include Caspase-1, NLRP3, IL-18 and IL-1β, etc. The GO and KEGG analyses revealed that BEL's mechanism of action involves the NLRP3 pathways. Molecular docking and molecular dynamics simulation indicated that BEL exhibits strong binding affinity for both Galectin-3 (Gal-3) and NLRP3. Western blot and immunohistochemistry staining further confirmed that BEL inhibited the expression of proteins in the Gal-3/NLRP3 signaling pathway. Conclusion: BEL may alleviate DOX-induced liver injury by inhibiting Gal-3/NLRP3-mediated pyroptosis.
Indexed as
Identifiers
42771163What 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.