Protective effects of avenanthramide-C against cisplatin-induced cardiotoxicity in rats by attenuating oxidative stress, inflammatory cytokines, and modulating p62–Keap1–Nrf2 pathway

AVN-C may protect against CIS-induced cardiotoxicity by reducing oxidative stress and inflammation, possibly activating the p62-Keap1-Nrf2 pathway. Histopathologically, heart tissues treated with CIS + AVN-C were less damaged than tissues treated with the CIS group. These findings suggest AVN-C as a promising therapeutic agent against CIS-induced cardiotoxicity. Nonetheless, the absence of echocardiographic assessments remains a key limitation, and future studies incorporating these evaluations are warranted to strengthen translational relevance.