Fig. 6

PDA NPs restrained the pro-inflammatory transformation of microglia via the TLR4/NF-κB signaling pathway. a Confocal fluorescence images showing the morphology of microglia. Inset of a: fluorescence image of single microglia under zoom and skeletonization. Scale bar = 50 μm (overview) and 5 μm (inset). Quantification of Iba1 ⁺ cell b solidity [F (3, 49) = 39.23, P < 0.0001] and c branch length [F (3, 47) = 5.904, P = 0.0017] (12 images from 3 mice in each group). d Representative western blot and e the corresponding bar graphs with dots showing TNF-α, IL-1β and CD86 expression levels in the hippocampus [TNF-α: F (3, 16) = 8.289, P = 0.0015; IL-1β: F (3, 16) = 5.384, P = 0.0094; CD86: F (3, 16) = 8.607, P = 0.0012] (n = 5/group). f The initial mechanism of PDA NPs restraining LPS induced microglial activation. g Representative western blot and h the corresponding bar graphs with dots showing TLR4, MyD88 and p-NF-κB p65 expression levels in the hippocampus [TLR4: F (3, 16) = 6.536, P = 0.0043; MyD88: F (3, 16) = 9.799, P = 0.0007; p-NF-κB p65: F (3, 16) = 16.35, P < 0.0001[ (n = 5/group). Data are presented as the means ± SEM. Results were analyzed by one-way ANOVA followed by Bonferroni test for post hoc comparisons. (*): P < 0.05, (**): P < 0.01 versus indicated groups. LPS lipopolysaccharide, PBS phosphate-buffered saline, PDA NPs polydopamine nanoparticles, TNF-α tumor necrosis factor alpha, IL1-β interleukin-1 beta, CD86 cluster of differentiation 86, TLR4 toll Like receptor 4, MyD88 myeloid differentiation factor 88, p-NF-κB phospho-nuclear factor kappa-B