Abstract
PURPOSE: The aim of this research study is to assess the ability of quercetin to protect the heart from the negative consequences of tacrolimus-induced cardiotoxicity. METHODS: A total of 30 rats were divided into 5 groups. Tacrolimus was used to induce cardiotoxicity, whereas quercetin was employed as a protective agent. RESULTS: Tacrolimus administration significantly raised the levels of serum cardiac biomarkers (Lactate dehydrogenase, creatine kinase-myocardial band, and troponin-I) as well as inflammatory biomarkers (tumor necrosis alpha and interleukin 6). The administration of quercetin reduced raised levels of cardiac and inflammatory biomarkers significantly. In addition, treatment with tacrolimus resulted in higher malondialdehyde (MDA) (lipid peroxidation marker) levels and falling in the levels of reduced glutathione (GSH) as well as antioxidant enzymes such as superoxide dismutase (SOD), glutathione reductase (GR), and catalase (CAT). Quercetin treatment significantly reduced MDA levels and increased GSH and antioxidant enzyme (SOD, GR, and CAT) levels. Moreover, the tacrolimus-administered group exhibited histological changes in cardiac tissue cited as vacuole formation, large and uncondensed nucleus, and cardiomyocyte hypertrophy. The quercetin treatment reduced the inflammatory cell infiltration in cardiac tissue and thus reduced vacuole formation and hypertrophy. CONCLUSIONS: The outcome showed quercetin's cardioprotective potential against tacrolimus-administered cardiotoxicity. Consequently, it is concluded that quercetin may be used as add-on therapy with tacrolimus to reduce cardiac adverse effects.