ArticleHistology and histopathology2026
Urolithin A mitigates doxorubicin-induced myocardial injury via suppression of ROS-driven apoptotic signaling.
Article in Histology and histopathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundDoxorubicin (DOX), as a broad-spectrum antitumor drug, achieved great success in the clinic. Nevertheless, severe adverse effects, in particular cardiac toxicity, significantly restrict its clinical utilization. Urolithin A (UA), a metabolite produced by the metabolic activity of intestinal microorganisms on pomegranates, exerts novel protective potential against cardiovascular disease. However, the inhibitory effect of UA against DOX-mediated cardiotoxicity has not been fully explored. Herein, the protective effect and mechanism of UA against DOX-induced cardiotoxicity
methodsThe effects of UA and DOX on cell activity and cell apoptosis were assessed by cell counting Kit-8 (CCK-8), flow cytometry, and Terminal deoxynucleotidyl transferase dUTP Nick End Labeling (TUNEL) staining. Reactive oxygen species (ROS) were examined by fluorescent probes. Protein expression was detected by western blotting. A cardiotoxicity rat model was established via injection of DOX to evaluate the
resultsDOX induced obvious ROS-mediated oxidative damage and ultimately led to H9c2 cell apoptosis
conclusionOur findings validated the rational design that UA has the potential to mitigate DOX-induced myocardial injury
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