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    Eugenol attenuates paclitaxel-induced cardiotoxicity by modulating autophagy-related markers in rats
    (Mashhad Univ Med Sciences, 2026) Yildiz, Halime Tozak; Kucukgunay, Sadik; Korkmaz, Oya; Kocak, Seda; Bucak, Mustafa Numan
    Objective(s): Paclitaxel (PTX) is a commonly used chemotherapeutic agent that causes cardiotoxicity characterized by oxidative stress, inflammation, and mitochondrial dysfunction, which disrupts autophagy and apoptosis in cardiomyocytes. This study investigated the therapeutic potential of eugenol (EUG), a natural anti-oxidant and anti-inflammatory compound, against PTX-induced cardiac damage. Materials and Methods: Thirty-six male Wistar rats were randomly assigned to six groups: Control, EUG5, EUG25, PTX, PTX+EUG5, and PTX+EUG25. Hemodynamic parameters (systolic and diastolic blood pressure and heart rate), serum cardiac biomarkers (troponin T and brain natriuretic peptide), histopathological alterations, and immunohistochemical expression of autophagy-related proteins (mTOR, ULK1, and Atg13) were evaluated. Results: PTX administration significantly reduced arterial blood pressure and increased serum cardiac injury biomarkers, accompanied by marked myocardial structural damage. Histopathological analysis revealed myocardial degeneration, inflammation, edema, and tissue disorganization in the PTX group. In PTX-exposed rats treated with EUG, arterial blood pressure was higher, and serum cardiac injury biomarkers were lower than in the PTX group, accompanied by reduced histopathological scores. PTX exposure was associated with decreased mTOR expression and increased ULK1 and Atg13 immunoreactivity, while EUG-treated PTX groups showed values closer to those of the control group for these autophagy-related markers. Conclusion: EUG administration was associated with reduced biochemical and histopathological indicators of cardiac injury in PTX-exposed rats, along with changes in autophagy-related markers. These findings demonstrate that EUG treatment coincided with attenuation of PTX-induced cardiac injury at the biochemical and histopathological levels, suggesting its potential experimental value in models of chemotherapy-associated cardiotoxicity.
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    Protective effects of rutin against docetaxel-induced testicular damage in rats: Effects on antioxidant defence, apoptosis and autophagy
    (Pergamon-Elsevier Science Ltd, 2026) Kucukgunay, Sadik; Yildiz, Halime Tozak; Korkmaz, Oya; Bolacali, Memis; Bucak, Mustafa Numan; Cay, Hasan Ali; Guler, Sohret
    Docetaxel (DTX), a widely used chemotherapeutic agent, is known for its effectiveness in cancer treatment but also for its toxic effects on healthy tissues, particularly the male reproductive system. This study aimed to investigate the protective role of rutin, a natural flavonoid with known antioxidant and anti-apoptotic properties, against DTX-induced testicular damage in rats. Thirty-six adult male Wistar rats were randomly divided into six groups: Control, Rutin 50 mg/kg (R50), Rutin 100 mg/kg (R100), DTX, DTX+R50, and DTX+R100. A single dose of DTX (30 mg/kg, i.p.) was administered, while rutin was given orally for 7 days. On day eight, all animals were sacrificed. Sperm parameters (concentration, motility, morphology, chromatin integrity), serum testosterone and inhibin B levels, and testicular MDA and SOD levels were assessed. Histological evaluations were conducted using hematoxylin-eosin staining, Johnsen scoring, and tubule diameter measurements. Immunohistochemical analysis of Caspase-3, Bax, Bcl-2, mTOR, ULK1, and Atg13 was performed. Data were analyzed, and p < 0.05 was considered statistically significant. DTX significantly impaired sperm motility and hormone levels, increased oxidative stress, and caused histological damage in the testes (p < 0.001). Rutin, especially at 100 mg/kg, ameliorated these effects, restoring sperm function, hormonal balance, and testicular architecture. Furthermore, rutin reduced DTX-induced apoptosis and autophagy marker expression while preserving Bcl-2 levels (p < 0.001). DTX induces structural and functional impairments in testicular tissue via oxidative stress, apoptosis, and autophagy. Rutin demonstrated a dose-dependent protective effect, suggesting its potential as a supportive agent against chemotherapy-induced gonadotoxicity.