Modulation of gastric mucosal inflammatory responses to Helicobacter pylori by ghrelin: Role of cNOS-dependent IKK- β S-nitrosylation in the regulation of COX-2 activation

摘要: Disturbances in nitric oxide synthase (NOS) and cyclooxygenase (COX) isozyme systems, manifested by the excessive NO prostaglandin (PGE2) generation, are well-recognized features of gastric mucosal inflammatory responses to H. pylori infection. In this study, we report that LPS-induced enhancement inducible (i) iNOS expression COX-2 activation was accompanied impairment constitutive (c) cNOS phosphorylation, up-regulation inhibitory κB kinase-β (IKKβ) increase transcriptional factor, NF-κB, nuclear translocation. Further, show abrogation control over NF-κB has lead induction through S-nitrosylation. Moreover, demonstrate modulatory effect peptide hormone, ghrelin, on changes reflected Src/Akt-dependent phosphorylation suppression IKK-β activity cNOS-mediated protein As a result, ghrelin exerted translocation, thus causing repression gene inhibition iNOS-dependent Our findings point as pivotal element signaling cascade which exerts proinflammatory events triggered mucosa