Obiective To investigate acid-suppression efficacy of proton pump inhibitors(PPls) in relation to CYP2C19 genetic polymorphism on patients with peptic ulcer. Methods By an open, randomized and control trial, fifty nine patients with active peptic ulcer were randomly assigned to receive one of three PPIs on a single dose (20 mg of each drug): omeprazole group (n=19), rabeprazole group (n=20) and esomeprazole group (n=20). lntragastric pH was recorded 1 hour before and 24 hours after administration. CYP2C19 genotype was tested in all patients. Resuits The EMs/PMs ratio of each group was 16/3,17/3 and 17/3, respectively. The total time that intragastric pH＞4, time percent pH＞4 and median pH in PMs patients were significantly higher than those in EMs patients of omeprazole group (P＜0.05). But all these differences were not found in rabeprazole group and esomeprazole group. The pH of nocturnal acid breakthrough (NAB) in both rabeprazole group and esomeprazole group was higher than that of omeprazole group, while there was no significant difference between rabeprazole group and esomeprazole group. Gonclusion The acid-suppression efficacy of omeprazole is highly dependent on CYP2C19 genetic polymorphism, while CYP2C19 genetic polymorphism may have a little influence on the acid-suppression efficacy of rabeprazole and esomeprazole. The acid-suppression action of rabeprazole and esomeprazole is superior to omeprazole, especially on night acid secretion.

Objective:To observe the effect of irradiation on the production of IL-8 in lung cancer cell line A549 and explore its possible mechanism.Methods:A549 cells irradiated with different doses of X-rays were used to collect cell supernatant, cellular RNA and protein at different time points after irradiation. The expression level of IL-8 mRNA in A549 cells after irradiation was detected by RT-PCR, which was further validated by real-time quantitative PCR. The expression level of IL-8 in the cell supernatant was quantitatively measured by ELISA. The expression levels of cellular signaling pathway molecules in A549 cells after irradiation were detected by Western Blot. The A549 cells were pretreated with p38 MAPK inhibitor, NF-κB inhibitor and ROS scavenger. The effect of these inhibitors on the expression of IL-8 in A549 cells induced by irradiation was evaluated by ELISA.Results:Irradiation up-regulated the expression of IL-8 in A549 cells in a dose-and time-dependent manner. Irradiation activated the p38 MAPK and NF-κB signaling pathway in A549 cells. p38 MAPK and NF-κB inhibitors blocked the induction of IL-8 of A549 cells by irradiation. Inhibition of ROS failed to inhibit the induction of IL-8 of A549 cells by irradiation.Conclusion:Irradiation can increase the production of IL-8 in lung cancer cells A549, possibly through the activation of p38 MAPK and NF-κB signaling pathways in a ROS-independent pattern.