M1905 Symptom Resolution in Uninvestigated Patients with Symptoms of Gastro-Oesophageal Reflux Treated with Rabeprazole or Esomeprazole: A Randomised Trial

Abstract

diacetate (DCF-DA) was used to detect the generation of intracellular ROS (especially H2O2). When the cells were exposed to IL-1beta (2.5, 5, 10, 25, 50 ng/mL) medium for 18 hours, cell viability did not show any change. We found that QGC did not reduce COX-2 expression induced by IL-1beta (25 ng/mL, 18 hrs), which plays an important role in inflammatory condition. However, QGC significantly inhibited the production of intracellular ROS induced by IL-1beta (25 ng/mL, 30 min). IL-1beta induced the activation of ERK, p38 MAPK and IB, and the nuclear translocation of NFkB, which were reversed by ROS scavenger Nactetylcysteine (NAC) and QGC, not by NADPH oxidase inhibitor diphenyleneiodonium (DPI). We also found that pretreatment of cells with ERK inhibitor PD98059, p38 MAPK inhibitor SB202190, NAC and QGC significantly attenuated the nuclear translocation of NFkB and the activation of IB induced by IL-1beta. Taken together, IL-1beta increases production of intracellular ROS and expression of COX-2, while it does not affect cell viability. QGC has a scavenger effect on cytokine-induced ROS production, thereby preventing its downstream events, the nuclear translocation of NFkB and the activation of IB, mediating by the activation of ERK and p38 MAPK, although QGC does not inhibit IL-1beta-stimulated COX-2 expression in feline esophageal epithelial cells.