Expression of NMDA receptor and microRNA-219 in rats submitted to cerebral ischemia associated with alcoholism
ABSTRACT Alcohol consumption aggravates injuries caused by ischemia. Many molecular mechanisms are involved in the pathophysiology of cerebral ischemia, including neurotransmitter expression, which is regulated by microRNAs. Objective: To evaluate the microRNA-219 and NMDA expression in brain tissue...
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Published in: | Arquivos de neuro-psiquiatria Vol. 75; no. 1; pp. 30 - 35 |
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Main Authors: | , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Rua do Matoso 170, Rio de Janeiro, RJ, CEP 20270-135, Brazil
Thieme Revinter Publicações Ltda
01-01-2017
Academia Brasileira de Neurologia - ABNEURO Academia Brasileira de Neurologia (ABNEURO) |
Subjects: | |
Online Access: | Get full text |
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Summary: | ABSTRACT
Alcohol consumption aggravates injuries caused by ischemia. Many molecular mechanisms are involved in the pathophysiology of cerebral ischemia, including neurotransmitter expression, which is regulated by microRNAs.
Objective:
To evaluate the microRNA-219 and NMDA expression in brain tissue and blood of animals subjected to cerebral ischemia associated with alcoholism.
Methods:
Fifty Wistar rats were divided into groups: control, sham, ischemic, alcoholic, and ischemic plus alcoholic. The expression of microRNA-219 and NMDA were analyzed by real-time PCR.
Results:
When compared to the control group, the microRNA-219 in brain tissue was less expressed in the ischemic, alcoholic, and ischemic plus alcoholic groups. In the blood, this microRNA had lower expression in alcoholic and ischemic plus alcoholic groups. In the brain tissue the NMDA gene expression was greater in the ischemic, alcoholic, and ischemic plus alcoholic groups.
Conclusion:
A possible modulation of NMDA by microRNA-219 was observed with an inverse correlation between them. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0004-282X 1678-4227 1678-4227 0004-282X |
DOI: | 10.1590/0004-282X20160188 |