Journal
ENVIRONMENTAL TOXICOLOGY
Volume 36, Issue 7, Pages 1389-1401Publisher
WILEY
DOI: 10.1002/tox.23134
Keywords
autophagy; cardiovascular toxicity; mechanism; oxidative stress; silica nanoparticles
Categories
Funding
- National Natural Science Foundation of China [81602893, 81973089]
- Natural Science Foundation of Jilin Province Science and Technology Department [20180101096JC]
- Natural Science Foundation of Shandong Province [ZR2015YL049]
- Key Research and Development Plan of Shandong Province [2018GSF118018]
- Medical and Health Technology Development Plan Project of Shandong Province [2016WS0540, 2018WSA18019]
- Jinan Science and Technology Project [201907022]
- Academic promotion programme of Shandong First Medical University [2019QL001]
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This study found that SiNPs induce cardiovascular toxicity through oxidative stress-mediated autophagy, and the Nrf2/HO-1 pathway negatively regulates autophagy.
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.
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