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. 2016 May 25;113(23):E3240–E3249. doi: 10.1073/pnas.1521453113

Fig. 1.

Fig. 1.

LC/MS/MS analysis of oxylipin-generating pathways in the mouse peritoneal cavity during acute inflammation and resolution initiated by zymosan A. (A) Absolute levels of oxylipins determined in naive peritoneal cavity lavage fluid of male C57BL/6 mice. (B) Sum of oxylipin-generated COX, CYP450, CYP450-lipoxygenase–like (CYP-L), or LO pathways using either arachidonic acid (AA), linoleic acid (LA), DHA, or EPA as a substrate in the naive peritoneal cavity. (C) Heatmap showing fold changes in oxylipin formation following zymosan A treatment (1 mg, i.p.) from 0 to 4 h (peak of acute inflammation), 24 h, and 48 h (resolution). (D and E) Fold-normalized square root of oxylipins produced by COX-AA (prostanoids), CYP-AA (DHETs), CYP-L-AA (19- and 20-HETE), CYP-DHA (19,20-EpDPE and 19,20-DiHDPA), CYP-EPA (17,18-DHEQ), and 5-LO-AA (5-HETE) pathways (D) and CYP-LA (EpOMEs and DiHOMEs), 8/12/15-LO (8-, 12-, and 15-HETE), and LO-LA (HODEs) pathways (E) in response to zymosan A over 48 h. Pathways in D and E represent two distinct responses to challenge with zymosan A. Data represent the mean ± SEM from n = 4–8 mice per group.