ArticleIranian journal of basic medical sciences2026
Quercetin attenuates ferroptosis-associated myocardial injury in rats after coronary microembolization by activating the Nrf2/HO-1 signaling pathway.
Article in Iranian journal of basic medical sciences, 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
Objectives: Coronary microembolization (CME) significantly contributes to the progression of heart failure and is strongly associated with adverse clinical outcomes in patients. Ferroptosis has been implicated in CME-induced myocardial injury. Quercetin has well-documented anti-inflammatory and antioxidant properties and shows therapeutic potential in coronary artery disease. However, its precise mechanism for regulating ferroptosis during CME-mediated myocardial injury remains unclear. This study aims to elucidate the therapeutic effects of quercetin and its underlying molecular mechanisms that regulate ferroptosis in cardiomyocytes following CME. Materials and Methods: The Sprague-Dawley(SD) rats were randomly divided into four groups (n=7 each): Sham, CME, CME+Quercetin (Que), and CME+Quercetin+ML385 (Que+ML385). The CME model was produced by injecting microspheres into the left ventricles. We administered pharmacological treatments as follows: The Que and Que+ML385 groups received daily oral quercetin (250 mg/kg) starting 7 days before model induction until the procedure day. Additionally, we pretreated the Que+ML385 group with intraperitoneal injection of ML385 (30 mg/kg) 2 hr before CME induction. The comprehensive evaluations include cardiac function assessment, quantification of serum biomarkers of myocardial injury, cardiac tissue histology, and analysis of ferroptosis-related molecular markers to evaluate quercetin's therapeutic effects. Results: Quercetin pretreatment significantly improved cardiac function, reduced serum markers of myocardial injury, and decreased microinfarction size. At the molecular level, quercetin up-regulated Nrf2 and HO-1 expression and attenuated biochemical markers of cardiomyocyte ferroptosis. However, ML385 co-treatment attenuated this protective effect. Conclusion: Quercetin may inhibit ferroptosis in cardiomyocytes by activating the Nrf2/HO-1 signaling pathway, thereby improving CME-related cardiac dysfunction and reducing myocardial injury.
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