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Fig. 6 | Molecular Neurodegeneration

Fig. 6

From: Intranasal insulin reverts central pathology and cognitive impairment in diabetic mother offspring

Fig. 6

Effect of insulin administration on central spontaneous bleeding and inflammation. a Cortical haemorrhage burden was significantly increased in DMO at P7 (**p < 0.01 vs. Control). By 10 weeks of age insulin administration significantly ameliorated this effect (**p < 0.01 vs. 0.01 vs. rest of the groups, ††p < 0.01 vs. Control, Control + ICV-Ins, Control + IN-Ins, ‡‡p < 0.01 vs. Control). A similar profile was observed when we measured hemorrahge density (P7: **p < 0.01 vs. Control; 10 weeks: **p < 0.01 vs. 0.01 vs. rest of the groups, ‡‡p < 0.01 vs. Control) while no differences were observed in hemorrhage size (P7: p < 0.053 vs. Control; 10 weeks p = 0.01 and no further differences were detected by Tuckey b test) (P7 n = 5 both groups, 10 weeks Control n = 5, Control + ICV-Ins n = 5, Control + IN-Ins n = 5, STZ n = 4, STZ + ICV-Ins n = 6 and STZ + IN-Ins n = 5). Hippocampal haemorrhage burden was increased in DMO and insulin administration reduced this effect by 10 weeks of age (P7: **p < 0.01 vs. Control; 10 weeks: ††p < 0.01 vs. Control, Control + ICV-Ins, Control + IN-Ins). A similar profile was observed in hemorrhage density although differences did not reach statistical significance at 10 weeks of age (P7: **p = 0.05 vs. Control, 10 weeks p = 0.165). No differences were observed in hemorrhage size (P7: p = 0.184; 10 weeks p = 0.410) (P7 n = 5 both groups, 10 weeks Control n = 5, Control + ICV-Ins n = 5, Control + IN-Ins n = 5, STZ n = 4, STZ + ICV-Ins n = 6 and STZ + IN-Ins n = 5). b Illustrative example of cortical haemorrhages at 10 weeks of age stained with Prussian blue. Scale bar = 500 μm. c Cortical microglia burden was increased at P7 (*p = 0.018 vs. Control) and insulin administration limited this effect in DMO at 10 weeks of age (**p < 0.01 vs. rest of the groups), microglia size (P7: **p < 0.01 vs. Control; 10 weeks **p < 0.01 vs. rest of the groups). A similar profile was observed in microglia density (P7: p = 0.166; 10 weeks **p < 0.01 vs. rest of the groups, ††p < 0.01 vs. Control, Control + ICV-Ins, Control + IN-Ins and STZ + IN-Ins) and microglia size (P7: **p < 0.01 vs. rest of the groups; 10 weeks **p < 0.01 vs. rest of the groups) (P7 Control n = 6 and STZ n = 5; 10 weeks Control n = 5, Control + ICV-Ins n = 5, Control + IN-Ins n = 4, STZ n = 5, STZ + ICV-Ins n = 3 and STZ + IN-Ins n = 3). A similar profile was observed for hippocampal microglia burden (P7: **p < 0.01 vs. Control; 10 weeks: **p < 0.01 vs. rest of the groups), density (P7: **p = 0.005 vs. Control; 10 weeks **p < 0.01 vs. rest of the groups) and size (P7: **p < 0.01 vs. Control; 10 weeks **p < 0.01 vs. rest of the groups) (P7 Control n = 4 and STZ n = 5, 10 weeks n = 5 in all groups). One-way ANOVA, followed by Tuckey b or Tamhane test, was used for statistical analysis. d Illustrative example of cortical microglia immunostaining with iba-1 antibody. Scale bar = 50 μm

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