Prophylactic Subacute Administration of Zinc Increases CCL2, CCR2, FGF2, and IGF-1 Expression and Prevents the Long-Term Memory Loss in a Rat Model of Cerebral Hypoxia-Ischemia

Figure 4

Effect of the subacute administration of zinc on CCR2 immunoreactivity after CCAO. Representative micrographs of CCR2 immunofluorescence ((a) to (o)) using a rabbit antibody against CCR2 and a goat antibody anti-rabbit IgG conjugated with fluorescein isothiocyanate (green color). The cerebral region was identified with propidium iodide (red color) counterstaining. Graphs ((p), (q), (r), (s), and (t)) show the normalized values of CCR2-IR with respect to control IR for CCAO (Figures 3(a) to 3(o)) and subacute administration of zinc ((a) to (o)). The IR was measured using ImageJ 1.45 of the National Institute of Health. CA, Cornu Ammonis, and DG, dentate gyrus, of the hippocampus. LV, layer V of the cerebral cortex. Plexus, choroid plexus. Values are expressed as the mean ± SEM from 3 rats for each experimental condition. , significant when compared with the control group; ANOVA test and post hoc Dunnett’s test. , significant when compared between groups; unpaired Student’s -test. .