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李宁, 陈祥娃, 霍婷婷, 等. 纳米二氧化硅通过PI3K/AKt信号通路影响肺泡巨噬细胞凋亡的研究[J]. koko体育app 学报（医学版）, 2020, 51(4): 488-493. DOI:
引用本文: 李宁, 陈祥娃, 霍婷婷, 等. 纳米二氧化硅通过PI3K/AKt信号通路影响肺泡巨噬细胞凋亡的研究[J]. koko体育app 学报（医学版）, 2020, 51(4): 488-493. DOI:
LI Ning, CHEN Xiang-wa, HUO Ting-ting, et al. Nano-silicon Dioxide Affects Apoptosis of Alveolar Macrophages via PI3K/AKt Signaling Pathway[J]. Journal of Sichuan University (Medical Sciences), 2020, 51(4): 488-493. DOI:
Citation: 💜 LI Ning, CHEN Xiang-wa, HUO Ting-ting, et al. Nano-silicon Dioxide Affects Apoptosis of Alveolar Macrophages via PI3K/AKt Signaling Pathway[J]. Journal of Sichuan University (Medical Sciences), 2020, 51(4): 488-493. DOI:

纳米二氧化硅通过PI3K/AKt信号通路影响肺泡巨噬细胞凋亡的研究

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

  • 摘要:
      目的  探讨磷脂酰肌醇激酶-3/蛋白激酶B（phosphatidyl inositol 3-kinase/protein kinase B，PI3K/AKt）信号通路对纳米二氧化硅（nano silica，NS）粉尘诱导肺泡巨噬细胞（alveolar macrophages，AM）凋亡发生的影响。
      方法  通过不同质量浓度的NS粉尘染毒AM细胞后，CCK-8法检测细胞存活率；荧光显微镜观察细胞形态；流式细胞术检测PI3K抑制剂LY294002预处理前后细胞的凋亡率与线粒体膜电位；Western blot法检测PI3K抑制剂LY294002预处理前后细胞凋亡相关蛋白Bax、Bcl-2以及磷酸化（p）-PI3K、p-AKt的表达水平。
      结果  NS可降低AM细胞的存活率，部分细胞出现凋亡形态学改变；LY294002预处理AM后，线粒体膜电位水平的下降程度增加，并下调Bcl-2、p-PI3K、p-AKt蛋白的表达，同时上调Bax蛋白的表达，增加细胞凋亡率。
      结论  PI3K/AKt信号通路可能参与了NS诱导AM细胞的凋亡过程。
     
    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.
     
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