Protective Role of UCP2 in Oxidative Stress and Apoptosis during the Silent Phase of an Experimental Model of Epilepsy Induced by Pilocarpine

Neuroprotection is a desirable process in many neurological disorders, yet complex mechanisms involved in this field are not completely understood. The pilocarpine epilepsy model causes potent, seizure-induced excitotoxicity cell death and mitochondria impairment. The present study is aimed at inves...

Full description

Saved in:
Bibliographic Details
Published in:Oxidative medicine and cellular longevity 2018-01, Vol.2018 (2018), p.1-12
Main Authors: Junior, José Antonio Silva, Naffah-Mazzacoratti, Maria da Graça, Serra, Andrey Jorge, Brigidio, Eduardo, Gouveia, Telma Luciana Furtado, Jacinto, Kalil Ribeiro, Feliciano, Regiane dos Santos, Dutra, Marina Rascio Henriques, Morris, Mariana
Format: Article
Language:English
Subjects:
Analysis
Animals
Apoptosis
Apoptosis - physiology
Brain research
Disease Models, Animal
Epilepsy
Kinases
Male
Neurosciences
Oxidative stress
Oxidative Stress - drug effects
Oxidative Stress - physiology
Pilocarpine
Rats
Rats, Wistar
RNA
Rodents
Seizures (Medicine)
Status Epilepticus - chemically induced
Status Epilepticus - metabolism
Status Epilepticus - pathology
Uncoupling Protein 2 - metabolism
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Neuroprotection is a desirable process in many neurological disorders, yet complex mechanisms involved in this field are not completely understood. The pilocarpine epilepsy model causes potent, seizure-induced excitotoxicity cell death and mitochondria impairment. The present study is aimed at investigating the role of UCP2, a ROS negative regulator, in the neuroprotection after cholinergic insult. Our data demonstrated that UCP2 expression was augmented in the rat hippocampus 3 days after status epilepticus (SE), reaching a peak on the fifth day, then returning to basal levels. Concomitantly, phospho-AKT expression levels were higher in the hippocampus during the early silent phase (5 days after SE). Additionally, it was demonstrated that the blockade of UCP2 by antisense oligonucleotides (ASO) in SE rats successfully diminished both UCP2 mRNA and protein contents. SE ASO rats presented increased mitochondrial proapoptotic factor expression, caspase-3 activity, inflammatory cytokine expression, and ROS formation. Moreover, ASO treatment diminished p-AKT expression and antioxidant enzyme activities after pilocarpine insult. In conclusion, the present results highlight the neuroprotective actions of UCP2, acting in the inhibition of apoptotic factors and oxidative stress, to increase neuron survival after SE onset.
ISSN:1942-0900
1942-0994
DOI:10.1155/2018/6736721