Nanoceria Nanozyme Attenuates CoCl ₂ ‐Induced Oxidative Stress and Mitochondrial Dysfunction in H9c2 Cardiomyoblasts

ABSTRACT The increasing prevalence of cardiovascular diseases (CVD) is strongly associated with oxidative stress and mitochondrial impairment that exacerbates myocardial ischemia and impairs cardiac function. Cerium oxide nanoparticles (nanoceria) are recognized for their unique intrinsic enzyme‐mimetic and antioxidant properties; however, their protective role against chemical stress induced by cobalt chloride (CoCl 2 ) remains poorly explored. In this study, we investigated the cytoprotective effects of nanoceria in CoCl 2 ‐exposed H9c2 cardiomyoblasts. Exposure to CoCl 2 significantly reduced cell viability, increased oxidative stress, upregulated expression of proapoptotic and proinflammatory markers, and downregulated antioxidant defense genes. Pretreatment with nanoceria significantly reduced CoCl 2 ‐induced cytotoxicity and oxidative stress while restoring the expression of antioxidant defense genes. Furthermore, nanoceria preserved mitochondrial membrane potential (MMP) and normalized the expression of genes related to mitochondrial biogenesis and dynamics. Notably, nanoceria suppressed the proapoptotic marker BNIP3 and increased the expression of anti‐apoptotic marker BCL‐2. Collectively, these findings highlight the therapeutic potential of nanoceria in mitigating CoCl 2 ‐induced oxidative damage and mitochondrial dysfunction in H9c2 cardiomyoblasts.