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Fig. 6 | Particle and Fibre Toxicology

Fig. 6

From: Lipophilic components of diesel exhaust particles induce pro-inflammatory responses in human endothelial cells through AhR dependent pathway(s)

Fig. 6

Effects of inhibitors on DEP-EOM-induced gene expression in HMEC-1. Cells were pre-treated with the anti-oxidant NAC (2 mM), the AhR inhibitor CH223191 (1.0 μM), or the PAR-2 inhibitor ENMD-1068 (2.5 mM) for 30 min prior to exposure to the lipophilic n-Hexane- (a) or DCM-soluble (b) fractions of DEP-EOM at a concentration corresponding to 50 μg/mL (7.5 μg/cm2) of native particles, or vehicle (DMSO) alone, for 5 h. Gene expression was measured by q-PCR. The mRNA levels are presented relative to gene expression in cells exposed to DMSO, represented by the dotted line at 1. The results are expressed as mean ± SEM (A/B: n = 3). *Statistically significant difference from unexposed controls. #Statistically significant difference from cells exposed to DEP-EOM

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