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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。“,”ObjectiveTo 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.MethodsAfter 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.ReslutsThe 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.ConclusionOur data suggested that the activation of PI3K/AKt signaling pathway played an important role in NS-induced apoptosis in alveolar macrophages.