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<p>Previous studies have shown that silica nanoparticles (SiNPs) can cause neuronal damage and neurodegenerative changes, but the specific mechanism remains incompletely understood. Using the mouse microglial BV-2 cell model, this study explored the neurotoxic mechanism of SiNPs from the perspectives of inflammation and autophagy. Results demonstrated that SiNPs exposure could reduce BV-2 cell viability, alter cell morphology, increase autophagosomes, elevate intracellular ROS levels and induce oxidative damage. It could also trigger inflammatory reactions associated with activation of the NLRP3 inflammasome. Inhibiting ROS can reduce the assembly and activation of the NLRP3 inflammasome. Furthermore, SiNPs might enhance cellular autophagy potentially via the CaMKK2/AMPKα/mTOR pathway. Inhibition of NLRP3 inflammasome could attenuate SiNPs induced inflammation and autophagy. Overall, this study confirms that SiNPs exert toxic effects on BV-2 cells, which may be associated with the excessive inflammation and autophagy they induce. SiNPs can enhance cellular autophagy via the CaMKK2/AMPKα/mTOR pathway, and the NLRP3 inflammasome plays a positive regulatory role in SiNPs induced autophagy in BV-2 cells.</p>

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Silica Nanoparticles Induce BV-2 Cells Autophagy Via activation of NLRP3 inflammasome and CaMKK2 Signaling Pathways

  • 期刊论文

  • 发表日期：

    2026年1月1日

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  • Tianxiang Liu,
  • Mingqian Wang,
  • Yuanyuan Zhang,
  • Li Yang,
  • Jia Zhang,
  • Hongzhu Wei,
  • Xinyue Li,
  • Huan Pang,
  • Jiali Li,
  • Zhixuan Luo,
  • Mengyue Liu,
  • Haiying Du,
  • Chao Zhao,
  • Xiuling Song,
  • Minghua Jin

摘要

Previous studies have shown that silica nanoparticles (SiNPs) can cause neuronal damage and neurodegenerative changes, but the specific mechanism remains incompletely understood. Using the mouse microglial BV-2 cell model, this study explored the neurotoxic mechanism of SiNPs from the perspectives of inflammation and autophagy. Results demonstrated that SiNPs exposure could reduce BV-2 cell viability, alter cell morphology, increase autophagosomes, elevate intracellular ROS levels and induce oxidative damage. It could also trigger inflammatory reactions associated with activation of the NLRP3 inflammasome. Inhibiting ROS can reduce the assembly and activation of the NLRP3 inflammasome. Furthermore, SiNPs might enhance cellular autophagy potentially via the CaMKK2/AMPKα/mTOR pathway. Inhibition of NLRP3 inflammasome could attenuate SiNPs induced inflammation and autophagy. Overall, this study confirms that SiNPs exert toxic effects on BV-2 cells, which may be associated with the excessive inflammation and autophagy they induce. SiNPs can enhance cellular autophagy via the CaMKK2/AMPKα/mTOR pathway, and the NLRP3 inflammasome plays a positive regulatory role in SiNPs induced autophagy in BV-2 cells.