Table 3.
Quantitation of plasma ATL (15-epi-lipoxin A4), LXA4, 12(R/S)-HETE, and 15(R/S)-HETE levels by chiral chromatography mass spectrometry in plasma from aspirin (10 mg/kg)- and LPS (10 mg/kg)-treated mice
| Component | Vehicle | Aspirin | LPS | LPS + aspirin |
|---|---|---|---|---|
| ATL (ng/ml) | ND | ND | ND | ND |
| LXA4 (ng/ml) | ND | ND | ND | ND |
| 12(S)-HETE (ng/ml) | ||||
| WT C57Bl/6 | 13.0 ± 2.2 | 12.0 ± 2.7 | 36.0 ± 7.3 | 38.2 ± 10.5* |
| COX-1−/− | 11.5 ± 1.3 | 10.7 ± 1.9 | 37.6 ± 5.8* | 35.4 ± 11.5 |
| COX-2−/− | 12.3 ± 3 | 11.1 ± 2.8 | 27.8 ± 13.7 | 36.8 ± 7.5 |
| 12(R)-HETE (ng/ml) | ND | ND | ND | ND |
| 15(S)-HETE (ng/ml) | ND | ND | ND | ND |
| 15(R)-HETE (ng/ml) | ND | ND | ND | ND |
ATL, LXA4, 12(R)-HETE, 15(S)-HETE, and 15(R)-HETE were not detectable (ND) in plasma from any tested treatment group and genotype of mice. 12(S)-HETE was detectable in all plasma samples and tended to be increased by LPS administration in all genotypes of mice, consistent with the ability of LPS to increase phospholipase A2 activity in vivo. Data are the means ± se for tissue from n = 4 mice aged 10–12 wk. Data were analyzed within each genotype using 1-way ANOVA followed by Bonferroni's multiple comparison test.
*
P < 0.05 vs. vehicle.