The Protective Effect of Quercetin-3-O-beta -D-Glucuronopyranoside on Ethanol-induced Damage in Cultured Feline Esophageal Epithelial Cells
- Authors
- Cho, Jung Hyun; Park, Sun Young; Lee, Ho Sung; Whang, Wan Kyunn; Sohn, Uy Dong
- Issue Date
- Dec-2011
- Publisher
- KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
- Keywords
- Flavonoid; Hydrogen peroxide; ERK; Esophageal epithelial cell; Ethanol
- Citation
- KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY, v.15, no.6, pp 319 - 326
- Pages
- 8
- Journal Title
- KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
- Volume
- 15
- Number
- 6
- Start Page
- 319
- End Page
- 326
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/21074
- DOI
- 10.4196/kjpp.2011.15.6.319
- ISSN
- 1226-4512
2093-3827
- Abstract
- Quercetin-3-O-beta -D-glucuronopyranoside (QGC) is a flavonoid glucoside extracted from Rumex Aquaticus Herba. We aimed to explore its protective effect against ethanol-induced cell damage and the mechanism involved in the effect in feline esophageal epithelial cells (EEC). Cell viability was tested and 2',7'-dichlorofluorescin diacetate assay was used to detect intracellular H2O2 production. Western blotting analysis was performed to investigate MAPK activation and interleukin 6 (IL-6) expression. Exposure of cells to 10% ethanol time-dependently decreased cell viability. Notably, exposure to ethanol for 30 min decreased cell viability to 43.4%. When cells were incubated with 50 mu M QGC for 12 h prior to and during ethanol treatment, cell viability was increased to 65%. QGC also inhibited the H2O2 production and activation of ERK 1/2 induced by ethanol. Pretreatment of cells with the NADPH oxidase inhibitor, diphenylene iodonium, also inhibited the ethanol-induced ERK 1/2 activation. Treatment of cells with ethanol for 30 or 60 min in the absence or presence of QGC exhibited no changes in the IL-6 expression or release compared to control. Taken together, the data indicate that the cytoprotective effect of QGC against ethanol-induced cell damage may involve inhibition of ROS generation and downstream activation of the ERK 1/2 in feline EEC.
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