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. 2019 Nov 2;33(12):14528–14541. doi: 10.1096/fj.201901570R

Figure 1.

Figure 1

Figure 1

The effect of volatile anesthetic isoflurane on the production of lipid mediators. A) Lipid mediator cascade derived from AAs. B, C). Mice were subjected to CLP surgery under ketamine/xylazine anesthesia, and then a group of mice were exposed to 1% isoflurane for 6 h. Peritoneal lavage fluid was collected at different time points after CLP surgery as indicated in figures. Lipid mediators originated from AAs were measured. Data were shown as means ± sd of 4 mice at each time point; n.s., not significant. Statistical analysis was performed using 1-way ANOVA with Bonferroni post hoc analysis. *P < 0.05, **P < 0.01, ***P < 0.001. 5-LOX–mediated lipid mediators were measured. 5-Hydroxyicosapentaenoic acid was a 5-LOX–derived lipid mediator from eicosapentaenoic acid. Other lipid mediators were 5-LOX derived from AAs. Data were shown as means ± sd of 4 mice at each time point; n.s., not significant. Statistical analysis was performed using 1-way ANOVA with Bonferroni post hoc analysis. *P < 0.05, **P < 0.01, ***P < 0.001 D). The role of LPS priming in the production of AA-derived lipid mediators was examined. Whole blood was primed with LPS (1 µg/ml) and stimulated with fMLP (0.1 µM). As a TLR4 inhibitor, TAK-242 (1 µM) was used. Isoflurane (ISF, 1%) was exposed to a group of samples. Data were shown as means ± sd of quadruplicates; n.s., not significant. Statistical analysis was performed using 1-way ANOVA with Bonferroni post hoc analysis. **P < 0.01, ***P < 0.001.