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Protective effects of Cirsium japonicum var. maackii against amyloid beta-induced neurotoxicity in C6 glial cellsopen access

Authors
김지현김민정최지명이상현조은주
Issue Date
Jun-2019
Publisher
충남대학교 농업과학연구소
Keywords
amyloid beta; apoptosis; Cirsium japonicum var. maackii; inflammation; oxidative stress
Citation
Korean Journal of Agricultural Science, v.46, no.2, pp 369 - 379
Pages
11
Journal Title
Korean Journal of Agricultural Science
Volume
46
Number
2
Start Page
369
End Page
379
URI
https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/36079
DOI
10.7744/kjoas.20190025
ISSN
2466-2402
2466-2410
Abstract
Alzheimer’s disease (AD) is the most common neurodegenerative disease associated with age, and amyloid beta (Aβ) is known to cause Alzheimer’s disease. In the present study, we investigated the protective effects of Cirsium japonicum var. maackii extract and its fractions against Aβ-induced neurotoxicity in C6 glial cells. The cells treated with Aβ25-35 showed a decrease in cell viability and an increase in reactive oxygen species (ROS) production compared with the non-treated cells. However, the cells treated with the C. japonicum var. maackii extract and its fractions increased the cell viability and inhibited the Aβ-induced ROS production. These results demonstrate the neuroprotective effects of C. japonicum var. maackii against Aβ. To further examine the protective mechanism, we measured inflammation and apoptosis related protein expressions. The cells treated with extract and fractions from C. japonicum var. maackii down-regulated inflammatory related proteins such as cyclooxygenase-2, interleukin (IL)-1β, and IL-6, and attenuated apoptosis related proteins including B-cell lymphoma-2 (Bcl-2) associated X protein/Bcl-2 ratio. In particular, the ethanol and ethylacetate fraction exhibited higher inhibitory effect against ROS production and apoptosis-related protein expressions among the extract and the other fractions. Therefore, this study demonstrated the protective effects of C. japonicum var. maackii extract and its fractions against Aβ-induced neurotoxicity in C6 glial cells through the regulation of oxidative stress, inflammation, and apoptosis, suggesting that it might have potential as a therapeutic for AD.
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