Excessive reactive oxygen species (ROS) and subsequent mitochondrial dysfunction are pivotal in initiating cardiac hypertrophy. To explore nano-selenium's (SeNP's) preventive potential against this condition, the authors evaluated chemically synthesized chitosan-SeNPs and biosynthesized YC-3-SeNPs in an angiotensin II (Ang II)-induced cardiac hypertrophy model. This investigation encompassed ROS measurement, mitochondrial membrane potential analysis, transmission electron microscopy, gene and protein expression analyses, protein carbonylation assays, serum antioxidant quantification and histological staining. SeNPs effectively countered Ang II-induced cardiac hypertrophy by reducing ROS, restoring mitochondrial and protein kinase 2α (CK2-α) function, activating antioxidant pathways and enhancing serum antioxidant levels. This finding underscores SeNPs' role in attenuating Ang II-induced myocardial hypertrophy both and .
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