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.
Highlights
Gyeongsang National University, Jinju, Korea 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
The middle cerebral artery occlusion (MCAO) surgical operation is used to induce cerebral ischemia that leads to infarct lesions and neuronal cell damage in a representative animal model [13,15]
This study demonstrated that there is a decrease in the expression of α-synuclein protein in MCAOinduced brain injury
Summary
Gyeongsang National University, Jinju, Korea 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. It is known that α-synuclein regulates neuronal survival, and low levels of α-synuclein expression result in cytotoxicity These results suggest that cerebral ischemic injury leads to a reduction in α-synuclein and causes serious brain damage. Cerebral ischemia is involved with various biochemical processes such as the generation of reactive oxygen species and excessive nitric acid, along with the activation of the inflammatory response and excitatory neurotransmitters [3,4,5] These changes trigger neuronal degeneration and neuronal cell death, leading to severe neuronal damage and neuronal dysfunction [6]. We investigated αsynuclein expression in both a cerebral ischemic animal model and neuronal cells damaged by glutamate treatment
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
