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.

中文翻译：

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Nrf2/HO-1 信号通路的激活减弱了 H9c2 细胞中二氧化硅纳米粒子诱导的 ROS 介导的自噬

二氧化硅纳米粒子（SiNPs）作为产量最高的纳米粉体之一，已广泛应用于各个领域。SiNPs 对生态生物和人类健康的不利影响越来越受到关注。SiNPs 的潜在心血管毒性和相关机制仍然难以捉摸。因此，在本研究中，我们研究了 SiNPs（60 nm）的心血管毒性，并使用H9c2探索了潜在机制心肌细胞。结果表明，SiNPs 诱导氧化应激并激活 Nrf2/HO-1 抗氧化途径。自噬也被 SiNPs 激活。有趣的是，N-乙酰-L-半胱氨酸（NAC）在抑制活性氧（ROS）后减弱了自噬。同时，Nrf2的下调增强了自噬。总之，这些数据表明SiNPs通过氧化应激诱导H9c2心肌细胞自噬， Nrf2/HO-1通路对自噬具有负调控作用，该研究为SiNPs的心血管毒性提供了新的证据，为未来纳米材料的安全使用提供了参考。