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. Author manuscript; available in PMC: 2009 Sep 26.

Published in final edited form as: Lipids. 2008 May 21;43(7):581–588. doi: 10.1007/s11745-008-3189-y

HCAEC were treated with either ethanol vehicle, 50 ng/mL TNF-α (light gray bars, ), or 50 µM 2-chlorohexadecanal (2-ClHDA) (striped bars, ) or 50 µM 2-chlorohexadecanoic acid (2-ClHA) (black bars, ) for the times indicated. Cells were scraped in lysis buffer, cDNA was prepared from purified mRNA, and samples were analyzed by quantitative PCR using primers for COX-2. Values (mean ± SEM) were normalized to GAPDH and expressed as fold increase over control-treated cells at each time point for three independent determinations. SEM of control values was less than 5% of the mean at all time points and there was no significant increase in control values over time, (* and **) represent p< 0.05 and p<0.01, respectively

Inline graphic — HCAEC were treated with either ethanol vehicle, 50 ng/mL TNF-α (light gray bars, ), or 50 µM 2-chlorohexadecanal (2-ClHDA) (striped bars, ) or 50 µM 2-chlorohexadecanoic acid (2-ClHA) (black bars, ) for the times indicated. Cells were scraped in lysis buffer, cDNA was prepared from purified mRNA, and samples were analyzed by quantitative PCR using primers for COX-2. Values (mean ± SEM) were normalized to GAPDH and expressed as fold increase over control-treated cells at each time point for three independent determinations. SEM of control values was less than 5% of the mean at all time points and there was no significant increase in control values over time, (* and **) represent p< 0.05 and p<0.01, respectively