The protective effect of sodium selenite against silver nanoparticles induced oxidative stress and autophagy in cardiomyocytes is associated with AMPK/mTOR signaling pathway.

Selenite(Se) is a trace mineral that is essential for cardiac health. This study aims to investigate the beneficial effects of Se on cardiomyocyte damage induced by silver nanoparticles (AgNPs) and to explore the underlying protective mechanisms. H9C2 cells were incubated with AgNPs with or without Se . Cell viability, reactive oxygen species (ROS), mitochondrial membrane potential, NAD⁺/NADH ratios, ATP levels, the mTOR signaling pathway, and autophagic proteins were measured. The results showed that AgNPs exposure significantly decreased cell viability, inhibited cell proliferation, and changed cell morphology. AgNPs dramatically elevated ROS production and descended mitochondrial membrane potential. Furthermore, the NAD⁺/NADH ratio and ATP level of the AgNPs exposure group were significantly lower than those of the control group. AgNPs activated AMPK, depressed mTOR, and increased LC3 II/I and P62(P < 0.05). Interestingly, treatment with Se effectively salvaged AgNPs-induced cardiomyocyte damage, reduced ROS accumulation, stabilized mitochondrial membrane potential, restored the NAD⁺/NADH ratio and ATP level, and prevented the activation of mTOR and autophagy dysfunction induced by AgNPs. Se mitigates AgNPs-induced cardiomyocyte damage by utilizing antioxidative properties and suppressing mitochondrial dysfunction mediated autophagy through regulating AMPK/mTOR signaling pathway.