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[Nano-silicon Dioxide Affects Apoptosis of Alveolar Macrophages via PI3K/AKt Signaling Pathway]
Ning Li1,2, Xiang-Wa Chen1, Ting-Ting Huo3
1Department of Laboratory Medicine, Affiliated Hospital of Southwest Medical University, Luzhou 646000, China.
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.
Insights
Nano-silica (NS) dust exposure induces alveolar macrophage (AM) apoptosis by activating the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway. Inhibiting this pathway increases AM apoptosis, highlighting its crucial role.
Area of Science:
- Toxicology
- Cell Biology
- Biochemistry
Background:
- Alveolar macrophages (AM) are crucial for lung immunity.
- Nano-silica (NS) exposure can induce AM apoptosis.
- The role of the PI3K/Akt pathway in NS-induced AM apoptosis requires clarification.
Purpose of the Study:
- To investigate the effect of the PI3K/Akt signaling pathway on nano-silica-induced apoptosis in alveolar macrophages.
- To elucidate the molecular mechanisms underlying NS toxicity in AM.
Main Methods:
- Exposure of AM to varying concentrations of NS.
- Assessment of AM viability using CCK-8 assay.
- Analysis of apoptosis, mitochondrial potential, and protein expression (Bax, Bcl-2, p-PI3K, p-Akt) via flow cytometry and Western blot.
- Pretreatment with PI3K inhibitor LY294002.
Main Results:
- NS exposure decreased AM survival in a time- and dose-dependent manner.
- LY294002 pretreatment reduced mitochondrial potential and p-PI3K/p-Akt/Bcl-2 expression.
- LY294002 pretreatment increased Bax expression and AM apoptosis rate.
Conclusions:
- Activation of the PI3K/Akt signaling pathway is critical in NS-induced AM apoptosis.
- Targeting the PI3K/Akt pathway may offer therapeutic strategies for NS-related lung injury.
