Cardioprotective Efficacy of Quercetin against Cardiotoxicity Induced by Different Diameters of Sphere Gold Nanoparticles (GNPs).

Background: Gold nanoparticles (GNPs) have garnered significant attention in the biomedicine field due to their exceptional electrical, mechanical, chemical, and optical characteristics. The interaction of these remarkable potentials with biological tissues carries a risk of toxicity. Quercetin (Qur) is a natural flavonoid and exhibits numerous pharmacological impacts, especially anti-inflammatory, anti-apoptotic, and antioxidant.

Objective: This investigation aimed to clarify the potential cardiotoxicity induced by different diameters of spherical GNPs as well as to evaluate the possible cardioprotective roles of Qur against the most toxic diameter of GNPs.

Methods: Rats were randomly grouped and treated with or without sphere GNPs (10, 20 and 50 nm) and Qur (200 mg/kg b.wt.). Heart and blood samples were collected and subjected to histological, immunohistochemical and biochemical investigations.

Results: When compared to the groups treated with 20 and 50 nm, the 10 nm GNPs dramatically increased the levels of cardiac biomarkers, including Troponin I, Creatine kinase isoenzyme-MB (CK-MB), CK-Total, lactate dehydrogenase (LDH). Histopathologically, 10 nm GNPs exhibited severe cardiomyocytes degenerations, atrophy, disorganization of myocardial fibers, focal hemorrhage, congested blood vessels and interstitial inflammatory cells infiltrations. Immunohistochemically, 10 nm GNPs exhibited strongly positive expressions against anti-caspase-3 antibody confirming extensive apoptosis of cardiomyocytes. However, the majority of these pathological changes were significantly improved upon Qur treatment.

Conclusion: The size of GNPs is crucial to their toxicological impact on cardiac tissues where 10 nm GNPs can induce severe histological damage, potent cytotoxicity, and apoptosis rather than larger particles. Otherwise, pre-co-treatment with Qur revealed a significant cardioprotective effect against GNPs cardiotoxicity.