Rutin attenuates iron overload induced-ferroptosis in rats' heart tissue

Area of Science:

• Biochemistry
• Cardiovascular Research
• Toxicology

Background:

• Rutin, a natural flavonoid, possesses antioxidant and iron-chelating properties.
• Iron overload and ionizing radiation (IR) can induce ferroptosis, a form of regulated cell death, in heart tissue.

Purpose of the Study:

• To investigate the protective effects of rutin against iron-overload and IR-induced ferroptosis in rat heart tissue.
• To evaluate rutin's impact on iron metabolism, oxidative stress markers, and key ferroptosis-related genes.

Main Methods:

• Rats were subjected to iron overload and/or IR, with groups receiving rutin or deferasirox treatments.
• Evaluated serum iron profiles, oxidative stress markers (MDA, GSH, NO), antioxidant enzyme activities (GPx, SOD), and gene expression (GPX4, Nrf2, DMT1, ACSL4, caspase3) via RT-qPCR.
• Histopathological examination of heart tissues was performed.

Main Results:

• Rutin treatment significantly decreased TIBC, ferritin, transferrin, hepcidin, MDA, and NO levels.
• Rutin significantly increased GSH levels, GPx and SOD activities.
• Rutin upregulated protective genes (GPX4, Nrf2) and downregulated detrimental genes (DMT1, ACSL4, caspase3), mitigating ferroptosis.

Conclusions:

• Rutin demonstrates significant ameliorative effects against iron-overload and IR-induced ferroptosis in rat hearts.
• Rutin modulates iron metabolism, enhances antioxidant defense, and regulates ferroptosis-associated gene expression.
• Rutin can be considered a potential therapeutic agent for attenuating ferroptosis.