Figure 6: Melatonin treatment reduces VEGFR1 levels in the brains of Aβ1–42-induced AD rats. (A, B) Bands from the western blot assays for VEGFR1 in the cortex (A) and hippocampus (B). (C) Quantitative analysis of VEGFR1 expression by western blot assay. Data are expressed as the mean ± SEM (n = 3 per group). *P < 0.05, **P < 0.01, vs. sham group; #P < 0.05, ##P < 0.01, vs. AD group; &P < 0.05, vs. AD + melatonin group (one-way analysis of variance followed by Bonferroni post hoc tests). (D–G) Immunofluorescence staining for VEGFR1 (red, stained by Alexa 594) in the cortex (D) and the hippocampal DG (E), CA1 (F), and CA3 (G) regions. VEGFR1 immunoreactivity was higher in the AD group than in the sham group, and was partially inhibited following melatonin treatment. Scale bar: 200 μm. A+M: AD + melatonin group; AD: Alzheimer’s disease; Aβ: AD group; Aβ1–42: amyloid-beta 1–42; CA1: cornu ammonis 1; CA3: cornu ammonis 3; CX: cortex; DAPI: 4′,6-diamidino-2-phenylindole; DG: dentate gyrus; HP: hippocampus; M: melatonin group; Sham: sham group; VEGFR1: vascular endothelial growth factor receptor 1.