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- Title
The protective mechanism of quercetin-3-O-β- d-glucuronopyranoside (QGC) in HO-induced injury of feline esophageal epithelial cells.
- Authors
Sohn, Uy; Lee, Se; Lee, Sung; Nam, Yoonjin; Hwang, Wan
- Abstract
Quercetin-3-O-β- d-glucuronopyranoside (QGC) is a flavonoid glucoside extracted from Rumex Aquaticus. Recent studies have shown that QGC exhibits anti-inflammatory, anti-oxidateve effect in vivo and cytoprotective effect in vitro. Reactive oxygen species (ROS), at low concentration, play role as a primary signal or second messenger, however, at high concentration, ROS are cytotoxic. In this study, we investigated the protective mechanism of QGC in HO-induced injury of Feline Esophageal Epithelial Cells. Primary-cultured feline esophagus cells were identified by an indirect immunofluorescent staining method using a cytokeratin monoclonal antibody. Cell viability was determined by the conventional MTT reduction assay. Western blot analysis was performed with specific antibodies to investigate the activation of MAPKs, NF-κB, and IκB-α, and the expression of COX-2. When the cells were exposed to 600 μM HO medium for 24 h, cell viability decreased to 54 %. However, when cells were pretreated with 50-150 μM QGC for 12 h, the viability of cells exposed to HO significantly increased in the dose dependent manner. QGC (50 μM, 12 h) also inhibited the expression of COX-2 induced by 10 μM HO for 24 h. We found that treatment of HO activated p38 MAPK and JNK, but not ERK. However QGC inhibited the HO-induced p38 MAPK and JNK phosphorylation. In addition, NF-κB was activated by HO and translocated into the nucleus, but QGC inhibited the activation of NF-κB by blocking degradation of IκB. These data suggest that QGC reduces HO-induced COX-2 production by modulating the p38 MAPK, JNK, NF-κB signal pathway in feline esophageal epithelial cells.
- Publication
Archives of Pharmacal Research, 2016, Vol 39, Issue 9, p1324
- ISSN
0253-6269
- Publication type
Article
- DOI
10.1007/s12272-016-0808-7