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
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 e...
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| Format: | Article |
| Language: | English |
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Wiley
2015-01-01
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| Series: | Neural Plasticity |
| Online Access: | http://dx.doi.org/10.1155/2015/375391 |
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| author | Victor Manuel Blanco-Alvarez Guadalupe Soto-Rodriguez Juan Antonio Gonzalez-Barrios Daniel Martinez-Fong Eduardo Brambila Maricela Torres-Soto Ana Karina Aguilar-Peralta Alejandro Gonzalez-Vazquez Constantino Tomás-Sanchez I. Daniel Limón Jose R. Eguibar Araceli Ugarte Jeanett Hernandez-Castillo Bertha Alicia Leon-Chavez |
| author_facet | Victor Manuel Blanco-Alvarez Guadalupe Soto-Rodriguez Juan Antonio Gonzalez-Barrios Daniel Martinez-Fong Eduardo Brambila Maricela Torres-Soto Ana Karina Aguilar-Peralta Alejandro Gonzalez-Vazquez Constantino Tomás-Sanchez I. Daniel Limón Jose R. Eguibar Araceli Ugarte Jeanett Hernandez-Castillo Bertha Alicia Leon-Chavez |
| author_sort | Victor Manuel Blanco-Alvarez |
| collection | DOAJ |
| 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 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. |
| format | Article |
| id | doaj-art-3333be089a344ffab0292d90201e4bcf |
| institution | Kabale University |
| issn | 2090-5904 1687-5443 |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Neural Plasticity |
| spelling | doaj-art-3333be089a344ffab0292d90201e4bcf2025-02-03T05:51:55ZengWileyNeural Plasticity2090-59041687-54432015-01-01201510.1155/2015/375391375391Prophylactic 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-IschemiaVictor Manuel Blanco-Alvarez0Guadalupe Soto-Rodriguez1Juan Antonio Gonzalez-Barrios2Daniel Martinez-Fong3Eduardo Brambila4Maricela Torres-Soto5Ana Karina Aguilar-Peralta6Alejandro Gonzalez-Vazquez7Constantino Tomás-Sanchez8I. Daniel Limón9Jose R. Eguibar10Araceli Ugarte11Jeanett Hernandez-Castillo12Bertha Alicia Leon-Chavez13Facultad de Ciencias Químicas, BUAP, 14 Sur y Avenida San Claudio, 72570 Puebla, PUE, MexicoFacultad de Ciencias Químicas, BUAP, 14 Sur y Avenida San Claudio, 72570 Puebla, PUE, MexicoLaboratorio de Medicina Genómica, Hospital Regional 1° de Octubre, ISSSTE, Avenida Instituto Politécnico Nacional No. 1669, 07760 México, DF, MexicoDepartamento de Fisiología, Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Apartado Postal 14-740, 07000 México, DF, MexicoFacultad de Ciencias Químicas, BUAP, 14 Sur y Avenida San Claudio, 72570 Puebla, PUE, MexicoFacultad de Ciencias Químicas, BUAP, 14 Sur y Avenida San Claudio, 72570 Puebla, PUE, MexicoFacultad de Ciencias Químicas, BUAP, 14 Sur y Avenida San Claudio, 72570 Puebla, PUE, MexicoFacultad de Ciencias Químicas, BUAP, 14 Sur y Avenida San Claudio, 72570 Puebla, PUE, MexicoFacultad de Ciencias Químicas, BUAP, 14 Sur y Avenida San Claudio, 72570 Puebla, PUE, MexicoFacultad de Ciencias Químicas, BUAP, 14 Sur y Avenida San Claudio, 72570 Puebla, PUE, MexicoInstituto de Fisiología, BUAP, 14 Sur 6301, 72570 Puebla, PUE, MexicoInstituto de Fisiología, BUAP, 14 Sur 6301, 72570 Puebla, PUE, MexicoFacultad de Ciencias Químicas, BUAP, 14 Sur y Avenida San Claudio, 72570 Puebla, PUE, MexicoFacultad de Ciencias Químicas, BUAP, 14 Sur y Avenida San Claudio, 72570 Puebla, PUE, MexicoProphylactic 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.http://dx.doi.org/10.1155/2015/375391 |
| spellingShingle | Victor Manuel Blanco-Alvarez Guadalupe Soto-Rodriguez Juan Antonio Gonzalez-Barrios Daniel Martinez-Fong Eduardo Brambila Maricela Torres-Soto Ana Karina Aguilar-Peralta Alejandro Gonzalez-Vazquez Constantino Tomás-Sanchez I. Daniel Limón Jose R. Eguibar Araceli Ugarte Jeanett Hernandez-Castillo Bertha Alicia Leon-Chavez 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 |
| 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 |
| title_full | 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 |
| title_fullStr | 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 |
| title_full_unstemmed | 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 |
| title_short | 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 |
| title_sort | 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 |
| url | http://dx.doi.org/10.1155/2015/375391 |
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