Activation of Nrf2/HO-1 signaling pathway attenuates ROS-mediated autophagy induced by silica nanoparticles in H9c2 cells

Silica nanoparticles (SiNPs) as one of the most productive nano-powder, has been extensively applied in various fields. There has been increasing concern about the adverse effects of SiNPs on the health of ecological organisms and human. The potential cardiovascular toxicity of SiNPs and involved mechanisms remain elusive. Hence, in this study, we investigated the cardiovascular toxicity of SiNPs (60 nm) and explored the underlying mechanisms using H9c2 cardiomyocytes. Results showed that SiNPs induced oxidative stress and activated the Nrf2/HO-1 antioxidant pathway. Autophagy was also activated by SiNPs. Interestingly, N-acetyl-L-cysteine (NAC?attenuated autophagy after inhibiting reactive oxygen species (ROS). Meanwhile, down-regulation of Nrf2 enhanced autophagy. In summary, these data indicated that SiNPs induce autophagy in H9c2 cardiomyocytes through oxidative stress, and the Nrf2/HO-1 pathway has a negative regulatory effect on autophagy. This study provides new evidence for the cardiovascular toxicity of SiNPs and provides a reference for the safe use of nanomaterials in the future.

Automated summary

This study found that SiNPs induce cardiovascular toxicity through oxidative stress-mediated autophagy, and the Nrf2/HO-1 pathway negatively regulates autophagy.