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

• Published in: Journal of neural transplantation & plasticity 2015-01, Vol.2015 (2015), p.514-528-043
• Main Authors: Blanco-Alvarez, Victor Manuel, Soto-Rodriguez, Guadalupe, Gonzalez-Barrios, Juan Antonio, Martinez-Fong, Daniel, Brambila, Eduardo, Torres-Soto, Maricela, Aguilar-Peralta, Ana Karina, Gonzalez-Vazquez, Alejandro, Tomás-Sanchez, Constantino, Limón, I. Daniel, Eguibar, Jose R., Ugarte, Araceli, Hernandez-Castillo, Jeanett, Leon-Chavez, Bertha Alicia
• Format: Article
• Language: English
• Subjects: Animals; Antibodies; Binding sites; Brain; Carotid arteries; Carotid Stenosis - psychology; Cerebral ischemia; Chemokine CCL2 - biosynthesis; Chemokines; Chlorides - therapeutic use; Cytokines; Fibroblast Growth Factor 2 - biosynthesis; Fibroblast growth factors; Gene expression; Hypoxia; Hypoxia-Ischemia, Brain - drug therapy; Hypoxia-Ischemia, Brain - psychology; Insulin-Like Growth Factor I - biosynthesis; Insulin-like growth factors; Ischemia; Laboratory animals; Male; Maze Learning - drug effects; Memory Disorders - etiology; Memory Disorders - prevention & control; Memory, Disorders of; Memory, Long-Term - drug effects; Proteins; Rats; Rats, Wistar; Receptors, CCR2 - biosynthesis; Rodents; Zinc Compounds - therapeutic use; Zinc in the body
• ISSN: 0792-8483; 2090-5904; 1687-5443
• DOI: 10.1155/2015/375391

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 ZnCl2 (one dose every 24 h during four days); (2) Zn96h + CCAO, rats treated with ZnCl2 before 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.