Cerebral ischemic injury decreases α-synuclein expression in brain tissue and glutamate-exposed HT22 cells / 한국실험동물학회지
Laboratory Animal Research
;
: 244-250, 2017.
Article
in English
| WPRIM
| ID: wpr-101374
ABSTRACT
α-Synuclein is abundantly expressed in neuronal tissue, plays an essential role in the pathogenesis of neurodegenerative disorders, and exerts a neuroprotective effect against oxidative stress. Cerebral ischemia causes severe neurological disorders and neuronal dysfunction. In this study, we examined α-synuclein expression in middle cerebral artery occlusion (MCAO)-induced cerebral ischemic injury and neuronal cells damaged by glutamate treatment. MCAO surgical operation was performed on male Sprague-Dawley rats, and brain samples were isolated 24 hours after MCAO. We confirmed neurological behavior deficit, infarction area, and histopathological changes following MCAO injury. A proteomic approach and Western blot analysis demonstrated a decrease in α-synuclein in the cerebral cortices after MCAO injury. Moreover, glutamate treatment induced neuronal cell death and decreased α-synuclein expression in a hippocampal-derived cell line in a dose-dependent manner. It is known that α-synuclein regulates neuronal survival, and low levels of α-synuclein expression result in cytotoxicity. Thus, these results suggest that cerebral ischemic injury leads to a reduction in α-synuclein and consequently causes serious brain damage.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Brain
/
Cell Line
/
Cerebral Cortex
/
Brain Ischemia
/
Blotting, Western
/
Cell Death
/
Rats, Sprague-Dawley
/
Oxidative Stress
/
Neuroprotective Agents
/
Glutamic Acid
Limits:
Humans
/
Male
Language:
English
Journal:
Laboratory Animal Research
Year:
2017
Type:
Article
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