{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Blanco-Alvarez VM"],"funding":["Vicerrectoría de Investigación y Estudios de Posgrado"],"pagination":["375391"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4556331"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["2015"],"pubmed_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 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 d"],"journal":["Neural plasticity"],"pubmed_title":["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."],"pmcid":["PMC4556331"],"funding_grant_id":["NAT/2014"],"pubmed_authors":["Tomas-Sanchez C","Martinez-Fong D","Hernandez-Castillo J","Brambila E","Torres-Soto M","Gonzalez-Barrios JA","Soto-Rodriguez G","Gonzalez-Vazquez A","Blanco-Alvarez VM","Eguibar JR","Limon ID","Leon-Chavez BA","Ugarte A","Aguilar-Peralta AK"],"additional_accession":[]},"is_claimable":false,"name":"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.","description":"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 d","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015","modification":"2025-05-18T12:46:01.929Z","creation":"2025-05-18T12:46:01.929Z"},"accession":"S-EPMC4556331","cross_references":{"pubmed":["26355725"],"doi":["10.1155/2015/375391"]}}