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Figure 5 | Particle and Fibre Toxicology

Figure 5

From: Polycyclic aromatic hydrocarbon components contribute to the mitochondria-antiapoptotic effect of fine particulate matter on human bronchial epithelial cells via the aryl hydrocarbon receptor

Figure 5

The antiapoptotic effect is not correlated with proinflammatory cytokines release after PM 2.5 exposure. (A) Proinflammatory potential of different batches of PM2.5 10 μg/cm2 (AW, AS, VW and VS) on 16HBE cells. After 4 h or 24 h particle exposure, Amphiregulin (AR) and granulocyte monocyte colony-stimulating factor (GM-CSF) secretion were evaluated by ELISA. Data are represented as mean ± SD of triplicates. * indicates significance at p < 0.001, treated vs. control. (B) Flow cytometric analysis was done as before in the presence or absence of PM2.5-AW pretreatement and/or apoptosis inducer A23187 (3 μM). The implication of the EGFR was evaluated using the recombinant EGF ligand (rEGF 150 ng/ml) or the inhibitor AG1478 (1 μM). Data are represented as mean ± SD of three independent results (* treated vs. control p < 0.05; # vs. A23187 alone, p < 0.05).

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