Fig. 6: The dysregulated Kyn pathway causes oxidative stress in the fetal brain. | Nature Communications

Fig. 6: The dysregulated Kyn pathway causes oxidative stress in the fetal brain.

From: Disruption of tryptophan metabolism by high-fat diet-triggered maternal immune activation promotes social behavioral deficits in male mice

Fig. 6

a GSEA of activated oxidative stress pathway. b DHE staining of E18.5 fetal brain sections. c Statistical analysis of relative arbitrary unit of DHE staining (n = 9 slices from 3 mice; F 3,32 = 91.625, mCD vs mHFD: p = 2.2e-08, mHFD vs mH-Trp: p = 2.1e-06; mHFD vs mH-1MT: p = 2.3e-07). Maternal HFD significantly altered lipid profiles in the fetal forebrain (d) and resulted in the overproduction of oxidized lipids (e) (n = 6 mice/group). f 1-MT treatment alleviated the accumulation of oxidized lipids in the embryonic brain (n = 6 for each group). Data are represented as mean ± SD. In c p-values were determined by ANOVA with Bonferroni’s multiple comparison test. In a NES was calculated as described above. Statistical significance was determined using permutation testing (999 permutations), with FDR correction. In c, p-values were determined using one-way ANOVA, followed by Bonferroni’s correction for multiple comparisons. In d PERMANOVA by Adonis was used to determine statistical significance (F = 6.113, p = 0.007). In e a one-sample Kolmogorov-Smirnov test was used to assess the null hypothesis that the p-values for lipids in a set follow a reference uniform distribution. FDR correction was performed for the set-level p-values. The nomenclature of lipid classes in (e) is available at http://prime.psc.riken.jp. Source data are provided as a Source Data file.

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