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Neuroprotective effects of tumor necrosis factor-α inhibitor on rat hippocampal organotypic slice cultures treated with the 1-42 β-amyloidopen access쥐 해마 절편배양에서 β-아밀로이드 1-42분획 독성에 대한 종양괴사인자-α 억제제의 세포 보호 효과

Authors
허재혁현재경윤영철
Issue Date
2022
Publisher
Korean Society of Geriatric Neurology
Keywords
Alzheimer disease; Hippocampal slice culture; Beta-amyloid; Tumor necrosis factor inhibitors
Citation
Journal of Geriatric Neurology, v.1, no.1, pp 33 - 37
Pages
5
Journal Title
Journal of Geriatric Neurology
Volume
1
Number
1
Start Page
33
End Page
37
URI
https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/71605
DOI
10.53991/jgn.2021.00031
ISSN
2799-4090
2799-4104
Abstract
Background: Alzheimer disease (AD) is a chronic degenerative neuronal disease. Tumor necrosis factor (TNF) inhibitors involved in neuroinflammation in AD pathogenesis can be a potential treatment strategy for AD. Therefore, we performed organotypic hippocampal slice culture to investigate neuroprotective effects by TNF-α inhibitor from β-amyloid (Aβ)-induced neurotoxicity. Methods: We cultured the hippocampus of a 7 days postnatal Sprague-Dawley rats with 450 µm thick slices. The tissue slices had been exposed with 100 µM Aβ at an interval of 2 days since 14 days in vitro. Following co-treatment of the tissue slice with 100 µg/ml adalimumab and Aβ, we evaluated adalimumab effect on Aβ induced neurotoxicity by morphological observation of the hippocampus slice cultures with 1 µg/ml propidium iodide (PI) and measuring the expression levels of NeuN, Bcl2, and tau proteins. Results: Aβ (100 µM) induced increase of PI-positive fluorescence in the hippocampal slice. The adalimumab as a TNF-α inhibitor showed protective effects for Aβ-induced neurotoxicity, and reduced cell death of the CA1 region in hippocampal slice. The expression of NeuN and Bcl2 proteins was significantly decreased by 100 µM Aβ, and increased by co-treatment of 100 µg/ml adalimumab. Phosphorylation of tau protein increased by 100 µM Aβ and decreased by co-treatment of 100 µg/ml adalimumab. Conclusions: Adalimumab reduced the Aβ-induced neurotoxicity of the hippocampal slice culture, inhibited expression of NeuN, Bcl2 proteins and increasing of phophorylated tau protein. These findings would be useful as baseline data in the field of AD research and development of noble drugs for neurodegenerative diseases.
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