Fig. 7: N-Acetylcysteine supplementation rescues oxidative stress-induced neuronal migration deficits and offspring behavioral dysfunction.
a NAC supplementation schematic. b Measurement of the ratio of reduced to oxidized glutathione in the fetal brain (n = 6 mice/group; F 2,15 = 22.823, mCD vs mHFD: p = 0.045, mHFD vs mH-NAC: p = 1.41e-05). c The total antioxidant capacity of the mH-NAC fetal brain was significantly improved (n = 6 mice/group; F 2,15 = 86.955, mCD vs mHFD: p = 0.000507, mHFD vs mH-NAC: p = 2.74e-09). d GSEA of oxidative stress response (n = 3 for each group). e NAC inhibited superoxide production in the fetal brain (n = 9 slices from 3 mice; t = 11.028, p = 1.064145e-09). f Neuronal migration in fetal cortex (n = 9 slices from 3 mice; bin1: t = 3.893, p = 0.001; bin7: t = 2.256, p = 0.038; bin7: t = 2.256, p = 0.038; bin8: t = 3.714, p = 0.002; bin9: t = 3.324, p = 0.004). h NAC supplementation partially restored the distribution of Brn2-positive cells in the cerebral cortex (n = 9 slices from 3 mice; bin3: t = 2.903, p = 0.010; bin6: t = 2.786, p = 0.013; bin7: t = 3.548, p = 0.003; bin10: t = 4.388, p = 0.0004013904). A reduction in the total number of BrdU-positive (g) t = 2.694, p = 0.016) and Brn2-positive (i) t = 2.782, p = 0.013) neurons was observed in the mH-NAC fetal brain (n = 9 slices from 3 mice). j Offspring social behavior in three-chamber test (n = 10 mice, 10 litters/group; sociability: t = 3.318, p = 0.004; social preference: t = 5.259, p = 4.47265e-05). k Marble-burying test (n = 10 mice, 10 litters/group; t = 6.332, p = 4.469088e-06). Data are represented as mean ± SD. In b-c, p-values were determined by ANOVA with Dunnett’s multiple comparison test. The rest of the statistical significance was assessed by the two-sided unpaired Student’s t-test. Source data are provided as a Source Data file.
