Figure 7: Melatonin treatment reduces VEGFR2 levels in the brains of Aβ1–42-induced AD rats. (A, B) Bands from the western blot assays for VEGFR2 in the cortex (A) and hippocampus (B). (C) Quantitative analysis of VEGFR2 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 VEGFR2 (red, stained by Alexa 594) in the cortex (D) and the hippocampal DG (E), CA1 (F), and CA3 (G) regions. VEGFR2 immunoreactivity was higher in the AD group than in the sham group, and was partially prevented 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; VEGFR2: vascular endothelial growth factor receptor 2.