Fig. 4: Effects of CA-SBEβCD NPs treatment on AD-related pathology in the APP/PS1 mouse brain. | Cell Death & Disease

Fig. 4: Effects of CA-SBEβCD NPs treatment on AD-related pathology in the APP/PS1 mouse brain.

From: Inhibition of the CEBPβ-NFκB interaction by nanocarrier-packaged Carnosic acid ameliorates glia-mediated neuroinflammation and improves cognitive function in an Alzheimer’s disease model

Fig. 4

A Aβ-positive senile plaques were detected in APP/PS1 (Tg) mice and age-matched C57BL/6 (WT) mice treated with CA-SBEβCD NPs (loaded with 10 or 30 mg/kg of CA) or SBEβCD NPs (vehicle control) for 5 months. B The Aβ plaque density in the cerebral cortex and hippocampus was quantified. C Soluble Aβ40 and Aβ42 levels in the cortex were measured by ELISA. D Confocal laser scanning microscopy images showing apoptosis around Aβ-positive areas. TUNEL staining (green) showing apoptotic cells around Aβ plaques (red). DAPI was used to label the nuclei (blue). Scale bars: 100 μm. The white arrows indicate apoptotic cells. The high-magnification images in the right panels show the localisation of apoptotic cells around the Aβ-positive deposits. Scale bar = 60 μm. E Quantification of the apoptotic cells. F Western blot analysis showing the expression of the synaptic proteins, synapsin 1, PSD-95 and SYN. Blots were repeated at least three times for every condition.*p < 0.05, **p < 0.01 and ***p < 0.001 vs vehicle-treated mice by the one-way ANOVA (AE). *p < 0.05, **p < 0.01, ***p < 0.001 vs vehicle-treated mice; ###p < 0.001 vs the WT mice by the two-way ANOVA with post hoc Fisher’s least significant difference (LSD) tests. Values represent the mean ± SD. n = 8 in each group.

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