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Prophylactic Chronic Zinc Administration Increases Neuroinflammation in a Hypoxia-Ischemia Model
Joint Authors
Blanco-Alvarez, Victor Manuel
Martinez-Fong, Daniel
Gonzalez-Barrios, Juan Antonio
Brambila, Eduardo
Soto-Rodriguez, Guadalupe
Aguilar-Peralta, Ana Karina
Gonzalez-Vazquez, Alejandro
Tomás-Sanchez, Constantino
Limón, I. Daniel
Garcia-Robles, Guadalupe
Garate-Morales, José-Luis
Aguilar-Carrasco, Luis-Angel
Cebada, Jorge
Torres-Soto, Maricela
Leon-Chavez, Bertha Alicia
Source
Journal of Immunology Research
Issue
Vol. 2016, Issue 2016 (31 Dec. 2016), pp.1-15, 15 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2016-08-18
Country of Publication
Egypt
No. of Pages
15
Main Subjects
Abstract EN
Acute and subacute administration of zinc exert neuroprotective effects in hypoxia-ischemia animal models; yet the effect of chronic administration of zinc still remains unknown.
We addressed this issue by injecting zinc at a tolerable dose (0.5 mg/kg weight, i.p.) for 14 days before common carotid artery occlusion (CCAO) in a rat.
After CCAO, the level of zinc was measured by atomic absorption spectrophotometry, nitrites were determined by Griess method, lipoperoxidation was measured by Gerard-Monnier assay, and mRNA expression of 84 genes coding for cytokines, chemokines, and their receptors was measured by qRT-PCR, whereas nitrotyrosine, chemokines, and their receptors were assessed by ELISA and histopathological changes in the temporoparietal cortex-hippocampus at different time points.
Long-term memory was evaluated using Morris water maze.
Following CCAO, a significant increase in nitrosative stress, inflammatory chemokines/receptors, and cell death was observed after 8 h, and a 2.5-fold increase in zinc levels was detected after 7 days.
Although CXCL12 and FGF2 protein levels were significantly increased, the long-term memory was impaired 12 days after reperfusion in the Zn+CCAO group.
Our data suggest that the chronic administration of zinc at tolerable doses causes nitrosative stress, toxic zinc accumulation, and neuroinflammation, which might account for the neuronal death and cerebral dysfunction after CCAO.
American Psychological Association (APA)
Tomás-Sanchez, Constantino& Blanco-Alvarez, Victor Manuel& Gonzalez-Barrios, Juan Antonio& Martinez-Fong, Daniel& Garcia-Robles, Guadalupe& Soto-Rodriguez, Guadalupe…[et al.]. 2016. Prophylactic Chronic Zinc Administration Increases Neuroinflammation in a Hypoxia-Ischemia Model. Journal of Immunology Research،Vol. 2016, no. 2016, pp.1-15.
https://search.emarefa.net/detail/BIM-1108773
Modern Language Association (MLA)
Tomás-Sanchez, Constantino…[et al.]. Prophylactic Chronic Zinc Administration Increases Neuroinflammation in a Hypoxia-Ischemia Model. Journal of Immunology Research No. 2016 (2016), pp.1-15.
https://search.emarefa.net/detail/BIM-1108773
American Medical Association (AMA)
Tomás-Sanchez, Constantino& Blanco-Alvarez, Victor Manuel& Gonzalez-Barrios, Juan Antonio& Martinez-Fong, Daniel& Garcia-Robles, Guadalupe& Soto-Rodriguez, Guadalupe…[et al.]. Prophylactic Chronic Zinc Administration Increases Neuroinflammation in a Hypoxia-Ischemia Model. Journal of Immunology Research. 2016. Vol. 2016, no. 2016, pp.1-15.
https://search.emarefa.net/detail/BIM-1108773
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1108773