Abstract / Summary
The present study aimed to investigate the effects of chrysin on oxidative stress parameters and the ADMA/DDAH-1/NOS signaling pathway in rats with experimentally induced hyperthyroidism. In this study, 10–12-week-old male Sprague–Daw ley rats were used and randomly allocated into five groups: control, solvent, chrysin, hyperthyroid, and hyperthyroid + chrysin. Hyperthyroidism was induced by administration of L-thyroxine (0.3 mg/kg/day, i.p.) for eight weeks. Chrysin was administered orally by gavage at dose of 30 mg/kg/day. At the end of the experiment, body and heart weights were record ed, and serum fT3, fT4, and TSH levels were measured. In addition, ADMA, DDAH-1, and eNOS levels, as well as MDA, GSH, CAT, and GSH-Px levels in heart tissue were determined. In the hyperthyroid group, heart weight (p<0.001), serum fT3 (p<0.001) and fT4 (p<0.001) levels, and heart tissue MDA (p<0.01), ADMA (p<0.01), and eNOS (p<0.05) levels were significantly increased, whereas body weight (p<0.001), TSH (p<0.01), GSH (p<0.001), CAT (p<0.05), GSH-Px (p<0.01), and DDAH-1 (p<0.001) levels were significantly decreased. In the hyperthyroid + chrysin group, compared with the hyper thyroid group, heart weight (p<0.001), serum fT3 (p<0.01) and fT4 (p<0.001) levels, as well as heart tissue MDA (p<0.01) and eNOS (p<0.05) levels were decreased, while GSH-Px activity (p<0.01) was increased. Conclusion, hyperthyroidism induced increased oxidative stress in cardiac tissue and disrupted the ADMA/DDAH-1/NOS balance. Chrysin partially ameliorated these adverse alterations through its antioxidant effects and regulatory role in nitric oxide metabolism. These findings suggest that chrysin may represent a potential protective agent against hyperthyroidism-induced cardiac damage.