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

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Abstract

Prophylactic subacute administration of zinc decreases lipoperoxidation and cell death following a transient cerebral hypoxia-ischemia, thus suggesting neuroprotective and preconditioning effects. Chemokines and growth factors are also involved in the neuroprotective effect in hypoxia-ischemia. We explored whether zinc prevents the cerebral cortex-hippocampus injury through regulation of CCL2, CCR2, FGF2, and IGF-1 expression following a 10 min of common carotid artery occlusion (CCAO). Male rats were grouped as follows: (1) Zn96h, rats injected with ZnCl(one dose every 24 h during four days); (2) Zn96h + CCAO, rats treated with ZnClbefore CCAO; (3) CCAO, rats with CCAO only; (4) Sham group, rats with mock CCAO; and (5) untreated rats. The cerebral cortex-hippocampus was dissected at different times before and after CCAO. CCL2/CCR2, FGF2, and IGF-1 expression was assessed by RT-PCR and ELISA. Learning in Morris Water Maze was achieved by daily training during 5 days. Long-term memory was evaluated on day 7 after learning. Subacute administration of zinc increased expression of CCL2, CCR2, FGF2, and IGF-1 in the early and late phases of postreperfusion and prevented the CCAO-induced memory loss in the rat. These results might be explained by the induction of neural plasticity because of the expression of CCL2 and growth factors.

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Blanco-Alvarez, V. M., Soto-Rodriguez, G., Gonzalez-Barrios, J. A., Martinez-Fong, D., Brambila, E., Torres-Soto, M., … Leon-Chavez, B. A. (2015). 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. Neural Plasticity, 2015. https://doi.org/10.1155/2015/375391

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