[Nano-silicon Dioxide Affects Apoptosis of Alveolar Macrophages via PI3K/AKt Signaling Pathway]

Sichuan Da Xue Xue Bao Yi Xue Ban. 2020 Jul;51(4):488-493. doi: 10.12182/20200760103.
[Article in Chinese]

Abstract

Objective: To investigate the effect of phosphatidyl inositol 3-kinase/protein kinase B (PI3K/AKt) signaling pathway on the apoptosis of alveolar macrophages (AM) induced by nano-silica (NS) dust.

Methods: After exposure to different concentrations of NS suspension, CCK-8 assay was used to detect the AM viability; the cellular morphology of apoptotic AM was observed under fluorescence microscopy; the apoptosis rate and mitochondrial transmembrane potential of cells were detected by flow cytometry before and after pretreatment with phosphatidyl inositol 3-kinase (PI3K) inhibitor LY294002; Western blot was used to detect the expression of apoptosis-related proteins Bax, Bcl-2, p-PI3K and p-AKt.

Resluts: The survival rate of AM was decreased in a time-dose relationship after NS exposure. With LY294002 pretreatment, the mitochondrial transmembrane potential level and the expressions of p-PI3K, p-AKt and Bcl-2 were decreased, the expression of Bax and the apoptosis rate were increased.

Conclusion: Our data suggested that the activation of PI3K/AKt signaling pathway played an important role in NS-induced apoptosis in alveolar macrophages.

Keywords: Alveolar macrophages; Cell apoptosis; Nano-silica; PI3K/AKt.

MeSH terms

  • Apoptosis* / drug effects
  • Environmental Pollutants / toxicity
  • Humans
  • Macrophages, Alveolar* / drug effects
  • Macrophages, Alveolar* / enzymology
  • Phosphatidylinositol 3-Kinase* / metabolism
  • Proto-Oncogene Proteins c-akt* / metabolism
  • Signal Transduction* / drug effects
  • Silicon Dioxide* / toxicity

Substances

  • Environmental Pollutants
  • Silicon Dioxide
  • Phosphatidylinositol 3-Kinase
  • Proto-Oncogene Proteins c-akt