Hyperglycemia aggravates decrease in alpha-synuclein expression in a middle cerebral artery occlusion model.
10.5625/lar.2018.34.4.195
- Author:
Ju Bin KANG
1
;
Dong Kyun KIM
;
Dong Ju PARK
;
Murad Ali SHAH
;
Myeong Ok KIM
;
Eun Jung JUNG
;
Han Shin LEE
;
Phil Ok KOH
Author Information
1. Department of Anatomy, College of Veterinary Medicine, Research Institute of Life Science, Gyeongsang National University, Jinju, Korea. pokoh@gnu.ac.kr
- Publication Type:Original Article
- Keywords:
α-Synuclein;
hyperglycemia;
MCAO
- MeSH:
alpha-Synuclein*;
Animals;
Blotting, Western;
Brain;
Brain Injuries;
Brain Ischemia;
Cell Death;
Cerebral Cortex;
Cerebral Infarction;
Humans;
Hyperglycemia*;
Infarction, Middle Cerebral Artery*;
Injections, Intraperitoneal;
Male;
Middle Cerebral Artery*;
Neurodegenerative Diseases;
Neurons;
Neuroprotective Agents;
Polymerase Chain Reaction;
Rats, Sprague-Dawley;
Risk Factors;
Streptozocin;
Stroke
- From:Laboratory Animal Research
2018;34(4):195-202
- CountryRepublic of Korea
- Language:English
-
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.
