Fig. 7
The i.c.v. injection of AβOs induces brain inflammation. A Representative images of IBA-positive microglial cells at low and high resolutions (scale bar 300 and 50 µm, respectively) in the hippocampal CA1, CA3 and DG showing higher IR in the AD group. B Analysis of microglia altered morphology. Left panel: quantification of the IBA1-positive area in the DG and CA regions of the hippocampus and LEC. The number of branches (middle panel) and junctions (right panel) in microglial cell process per IBA1-positive cell was quantified in three regions (DG, CA and LEC). C Quantification of the GFAP-positive area in the CA and DG regions of the hippocampus. D Pearson’s correlation analysis indicates a strong positive correlation between the RR index and the level of IBA1-IR in the CA (E, left panel) and DG (E, right panel). E The relative mRNA expression of multiple inflammatory markers measured using qPCR. Data were normalized to two reference genes: ACTB and RPL13A. Data are presented as the means ± SEM. B–C and D n = 6 rats per group. *p < 0.05, ***p < 0.001. AD Alzheimer’s disease, DG dentate gyrus, CA cornu ammonis, IBA1 ionized calcium binding adaptor molecule 1, P2RY12 purinergic receptor P2Y12, TMEM119 transmembrane protein 119, IL6 interleukin 6, HIF1α hypoxia-inducible factor 1 α