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
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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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