Role of constitutive nitric oxide synthase in regulation of Helicobacter pylori-induced gastric mucosal cyclooxygenase-2 ac-tivation through S-nitrosylation: mechanism of ghrelin action

摘要: Gastric mucosal inflammatory responses to H. pylori lipopolysaccharide (LPS), are characterized by the excessive NO and prostaglandin (PGE2) generation due disturbances in nitric oxide synthase (NOS) cyclooxygenase (COX) systems. Here, we report that LPS-induced enhancement gastric inducible (i) iNOS) activity up-regulation PGE2 production was associated with suppression Akt kinase impairment constitutive (c) cNOS activation. The stimulatory effect of LPS on production, furthermore, susceptible COX-2 inhibitor, NS-398, iNOS 1400 W. Further, show countering peptide hormone, ghrelin, changes reflected up-regu- lation increase activation through phosphorylation, accompanied expression reduction loss protein S-nitrosylation. Moreover, ghre-lin S-nitrosylation subject repression inhibition. Our findings demonstrate induction in- fection leads S-nitro- sylation generation, ghrelin counters these untoward consequences Akt-mediated cNO- S required for gene repression.