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. Author manuscript; available in PMC: 2017 Aug 1.
Published in final edited form as: Placenta. 2016 Jun 11;44:61–68. doi: 10.1016/j.placenta.2016.06.004

Figure 3.

Figure 3

BaP does not affect TXB2 but leads to an induction of 6-keto PGF1α via the AHR/PTGS2 pathway. (A) EIA demonstrates that BaP increases 6-keto PGF1α concentrations in a dose-dependent manner, but this is inhibited in the setting of selective PTGS2 inhibition with NS398 (*p=0.001 in comparison to vehicle; ^p=0.007 in comparison to BaP 10−8 M treatment; #p<0.001 in comparison to BaP 10−6 M treatment). (B) Real-time PCR shows that BaP-mediated induction of PTGS2 mRNA expression is not inhibited with use of NS398, a selective inhibitor of PTGS2 activity (overall p=0.08 for one-way ANOVA). (C) A representative western blot from one subject also shows that PTGS2 protein expression is not inhibited by NS398 pre-treatment. (D) Graphical representation of western blot analyses from all subjects also confirms no effect of NS398 on PTGS2 protein expression (overall p=0.07 for one-way ANOVA). (E) AHR silencing via siRNA results in significant suppression of 6-keto PGF1α concentrations (*p<0.001 in comparison to control siRNA and vehicle; ^p<0.001 in comparison to control siRNA and BaP).