Table 2.
COX-1 or COX-2 deletion does not alter plasma levels of ATL (15-epi-lipoxin A4, measured by ELISA) in control or LPS-primed mice treated with aspirin
| Genotype | ATL (ng/ml) |
|||
|---|---|---|---|---|
| Vehicle | Aspirin | LPS | LPS + aspirin | |
| Diluted plasma | ||||
| WT C57Bl/6 | 1.2 ± 0.1 | 1 ± 0.2 | 1.6 ± 0.2 | 1.2 ± 0.1 |
| COX-1−/− | 1.5 ± 0.1 | 1.3 ± 0.1 | 1.4 ± 0.1 | 1.2 ± 0.1 |
| COX-2−/− | 1.5 ± 0.3 | 1.3 ± 0.2 | 1.6 ± 0.1 | 1.4 ± 0.1 |
| HPLC-extracted plasma | ||||
| WT C57Bl/6 | 1.9 ± 0.2 | 1.8 ± 0.2 | 2.3 ± 0.3 | 1.9 ± 0.3 |
| COX-1−/− | 1.7 ± 0.2 | 1.8 ± 0.1 | 2.0 ± 0.2 | 1.8 ± 0.2 |
| COX-2−/− | 2.1 ± 0.2 | 2.1 ± 0.2 | 2.1 ± 0.4 | 2.0 ± 0.3 |
Plasma ATL levels were not altered by aspirin (10 mg/kg), LPS, or COX-1/2 deletion when measured by commercial ELISA in plasma diluted in buffer or extracted using HPLC and C18 columns. Data are the means ± se for tissue from n = 8 mice aged 10–12 wk. Data were analyzed within each genotype using 1-way ANOVA followed by Bonferroni's multiple comparison test.