The protective mechanism of QGC in feline esophageal epithelial cells by interleukin-1ß treatment.

In a previous study, Quercetin-3-O-ß-D-glucuronopyranoside (QGC) has anti-oxidative and anti-inflammatory effects in vivo. QGC is a flavonoid glucoside extracted from Rumex Aquaticus. We investigated the downstream target proteins involved in IL-1ß-stimulated ROS production and the ability of QGC to inhibit ROS production. Cell viability was determined using the MTT reduction assay. Western blot analysis was performed with antibodies to investigate the activation of three MAPKs, NF-κB, and phosphorylated IκB-α (pIB), and the expression of COX-2. 2',7'-dichlorofluorescin diacetate was used to detect the generation of intracellular ROS species. When the cells were exposed to media containing IL-1ß for 18 h, cell viability was not affected. QGC did not reduce the COX-2 expression induced by IL-1ß. However; QGC attenuated the production of intracellular ROS induced by IL-1ß. IL-1ß increased the expression of ERK, p38 MAPK, and pIB, and nuclear translocation of NF-κB were recovered by the ROS scavenger N-acetyl-L-cysteine (NAC) and QGC, but not by the NADPH oxidase inhibitor diphenylene iodonium. Pretreatment of cells with the ERK inhibitor PD98059, the p38 MAPK inhibitor SB202190, NAC, and QGC attenuated nuclear translocation of NF-κB and activation of pIB. QGC has a scavenging effect on cytokine-induced ROS production, thereby preventing its downstream effects, nuclear translocation of NF-κB, and activation of pIB is mediated by activation of ERK and p38 MAPK, although QGC does not inhibit IL-1ß-stimulated COX-2 expression in feline esophageal epithelial cells. The data suggest that QGC exerts anti-oxidative effects and inhibitory effects against esophageal epithelial cells signals by the action of IL-1ß treatment.

The protective mechanism of quercetin-3-O-ß-D-glucuronopyranoside (QGC) in H2O2-induced injury of feline esophageal epithelial cells.

Quercetin-3-O-ß-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 H2O2-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 H2O2 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 H2O2 significantly increased in the dose dependent manner. QGC (50 µM, 12 h) also inhibited the expression of COX-2 induced by 10 µM H2O2 for 24 h. We found that treatment of H2O2 activated p38 MAPK and JNK, but not ERK. However QGC inhibited the H2O2-induced p38 MAPK and JNK phosphorylation. In addition, NF-κB was activated by H2O2 and translocated into the nucleus, but QGC inhibited the activation of NF-κB by blocking degradation of IκB. These data suggest that QGC reduces H2O2-induced COX-2 production by modulating the p38 MAPK, JNK, NF-κB signal pathway in feline esophageal epithelial cells.

The Inhibitory Effect of Quercetin-3-O-beta-D-Glucuronopyranoside on Gastritis and Reflux Esophagitis in Rats.

It was evaluated the inhibitory action of quercetin-3-O-beta-D-glucuronopyranoside (QGC) on reflux esophagitis and gastritis in rats. QGC was isolated from the herba of Rumex Aquaticus. Reflux esophagitis or gastritis was induced surgically or by administering indomethacin, respectively. Oral QGC decreased ulcer index, injury area, gastric volume, and acid output and increased gastric pH as compared with quercetin. Furthermore, QGC significantly decreased gastric lesion sizes induced by exposing the gastric mucosa to indomethacin. Malondialdehyde levels were found to increase significantly after inducing reflux esophagitis, and were reduced by QGC, but not by quercetin or omeprazole. These results show that QGC can inhibit reflux esophagitis and gastritis in rats.