Title: Su1930 Differences in Molecular Alterations and Cellular Phenotype in Background Mucosa of Early Gastric Cancer With and Without H. pylori Infection
Abstract: CRF injection), similar to stress, induced plasma corticosterone rise followed by the return of corticosterone level to baseline in 4 h after indomethacin administration.Indomethacininduced corticosterone rise was inhibited by NBI 27914 injection and these results confirm the critical role of CRF1 receptors in the activation of the HPA axis.Both astressin and astressin2-B injection resulted in a delay of the recovery to basal circulating corticosterone levels.The impaired termination of corticosterone response to indomethacin caused by astressin2-B was followed by aggravation of indomethacin-induced gastric injury.Conclusions: The results suggest that CRF injected into the periphery at the dose, which markedly increased plasma corticosterone levels, may induce protection against indomethacin-produced gastric injury through both CRF1 and CRF2 receptors.CRF2 receptor signaling pathway contributes to the appropriate termination of indomethacin-induced corticosterone secretion and the maintainance of gastric mucosal integrity during ulcerogenic action of indomethacin in rats.
Publication Year: 2014
Publication Date: 2014-05-01
Language: en
Type: article
Indexed In: ['crossref']
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