Our results show that the prophylactic subacute administration of zinc causes a neuroprotective effect in the hippocampus and cerebral cortex, by increasing the expression of neurotrophic factors CCL2, CCR2, FGF2, and IGF-1 in the early and late phases after transient hypoxia-ischemia process and preventing the loss of the long-term in spatial reference memory as evaluated in the Morris Water Maze. Here, CCL2 is linked to ischemia.