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Table 1 Krill oil (KO) supplementation increased the metabolites involved in pro-resolving pathways, particularly the biosynthesis of E-series resolvins. Fold change was calculated based on normalized peak intensities in Citrobacter rodentium induced colitis mice (CM) divided by those in healthy control mice (Down dysregulation) or those in KO divided by CM (Up dysregulation). Pathway: A: aspirin triggered resolvin E biosynthesis; B, aspirin-triggered lipoxin biosynthesis; C, lipoxin biosynthesis; and D, leukotriene biosynthesis

From: Mechanistic insights into the attenuation of intestinal inflammation and modulation of the gut microbiome by krill oil using in vitro and in vivo models

Metabolite Pathway* Fold change P value Dysregulation m/z RT
(5S)-HPETE D* 0.33 0.0004 Down 381.2270 3.974
(15R)-hydroxyeicosapentaenoate B*, C** 0.36 0.0022 Down 365.2321 4.474
(5S)-HPETE D* 0.40 0.0024 Down 395.2428 5.266
(5Z,8Z,11Z,14Z,17Z)-icosapentaenoate A** 0.20 0.0037 Down 347.2217 7.754
15 [epi-] lipoxin A4/B4 B*, C** 0.37 0.0031 Down 411.2375 4.481
18R-hydroxy-eicosapentaenoate A**, C**, D* 0.34 0.0020 Down 363.2167 4.736
5S hydro(peroxy),18R-hydroxy-eicosapentaenoate A** 0.25 0.0009 Down 349.2010 5.702
Resolvin E1 A** 0.29 0.0023 Down 409.2217 3.840
15S-hydroxypentaenoate B**, C*** 1.70 0.0406 Up 340.2020 9.158
leukotriene A4 A*, B**, C*** 1.68 0.0067 Up 363.2167 5.253
Resolvin E2 A*, B**, C*** 1.79 0.0315 Up 315.1957 7.663
  1. m/z mass-to-charge ratio, RT retention time in min
  2. ***p < 0.001; **p < 0.01; *p < 0.05.