Hyperglycemia aggravates decrease in alpha-synuclein expression in a middle cerebral artery occlusion model / 한국실험동물학회지
Laboratory Animal Research
;
: 195-202, 2018.
Article
in English
| WPRIM
| ID: wpr-718849
ABSTRACT
Hyperglycemia is one of the major risk factors for stroke. Hyperglycemia can lead to a more extensive infarct volume, aggravate neuronal damage after cerebral ischemia. α-Synuclein is especially abundant in neuronal tissue, where it underlies the etiopathology of several neurodegenerative diseases. This study investigated whether hyperglycemic conditions regulate the expression of α-synuclein in middle cerebral artery occlusion (MCAO)-induced cerebral ischemic injury. Male Sprague-Dawley rats were treated with streptozotocin (40 mg/kg) via intraperitoneal injection to induce hyperglycemic conditions. MCAO were performed four weeks after streptozotocin injection to induce focal cerebral ischemia, and cerebral cortex tissues were obtained 24 hours after MCAO. We confirmed that MCAO induced neurological functional deficits and cerebral infarction, and these changes were more extensive in diabetic animals compared to non-diabetic animals. Moreover, we identified a decrease in α-synuclein after MCAO injury. Diabetic animals showed a more serious decrease in α-synuclein than non-diabetic animals. Western blot and reverse-transcription PCR analyses confirmed more extensive decreases in α-synuclein expression in MCAO-injured animals with diabetic condition than these of non-diabetic animals. It is accepted that α-synuclein modulates neuronal cell death and exerts a neuroprotective effect. Thus, the results of this study suggest that hyperglycemic conditions cause more serious brain damage in ischemic brain injuries by decreasing α-synuclein expression.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Brain
/
Brain Injuries
/
Cerebral Cortex
/
Cerebral Infarction
/
Brain Ischemia
/
Blotting, Western
/
Polymerase Chain Reaction
/
Risk Factors
/
Cell Death
/
Rats, Sprague-Dawley
Type of study:
Etiology study
/
Prognostic study
/
Risk factors
Limits:
Animals
/
Humans
/
Male
Language:
English
Journal:
Laboratory Animal Research
Year:
2018
Type:
Article
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