Protective effects of kaempferol, quercetin, and its glycosides on amyloid beta-induced neurotoxicity in C6 glial cellopen access
- Authors
- Kim, J.H.; Kim, H.Y.; Cho, E.J.
- Issue Date
- 2019
- Publisher
- Korean Society for Applied Biological Chemistry
- Keywords
- Kaempferol-3-O-glucoside; Keampferol; Neurotoxicity; Quercetin; Quercetin-3-β-D-glucoside
- Citation
- Journal of Applied Biological Chemistry, v.62, no.4, pp 327 - 332
- Pages
- 6
- Indexed
- SCOPUS
KCI
- Journal Title
- Journal of Applied Biological Chemistry
- Volume
- 62
- Number
- 4
- Start Page
- 327
- End Page
- 332
- URI
- https://scholarworks.gnu.ac.kr/handle/sw.gnu/10638
- DOI
- 10.3839/jabc.2019.045
- ISSN
- 1976-0442
2234-7941
- Abstract
- Alzheimer’s disease (AD) is a common neurodegenerative disease. Oxidative stress by amyloid beta peptide (Aβ) of neuronal cell is the most cause of AD. In the present study, protective effects of several flavonoids such as kaempferol (K), kaempferol-3-O-glucoside (KG), quercetin (Q) and quercetin3-β-D-glucoside (QG) from Aβ25-35 were investigated using C6 glial cell. Treatment of Aβ25-35 to C6 glial cell showed decrease of cell viability, while treatment of flavonoids such as Q and QG increased cell viability. In addition, treatment of flavonoids declined reactive oxygen species (ROS) production compared with Aβ25-35induced control. The ROS production was increased by treatment of Aβ25-35 to 133.39%, while KG and QG at concentration of 1 ?M decreased ROS production to 107.44 and 113.10%, respectively. To study mechanisms of protective effect of these flavonoids against Aβ25-35, the protein expression related to inflammation under Aβ25-35-induced C6 glial cell was investigated. The results showed that C6 glial cell under Aβ25-35-induced oxidative stressup-regulated inflammation-related protein expressions. However,treatment of flavonoids led to reduction of protein expression suchas inducible nitric oxide synthase, cyclooxygenase-2 andinterleukin-1β. Especially, treatment of KG and QG decreasedmore effectively inflammation-related protein expression than itsaglycones, K and Q. Therefore, the present results indicated thatK, Q and its glycosides attenuated Aβ25-35-induced neuronal oxidative stress and inflammation. ? The Korean Society for Applied Biological Chemistry 2019.
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