Effects Of Chronic Helicobacter Pylori Infection On Expression Of IKK-β, NF-κB, XIAP In Gastric Epithelial Cells

H.pylori (Helicobacter pylori) infection is closely associated with occurance of human chronic gastritis, peptic ulcer disease and gastric adenocarcinoma . H.pylori has been classified as a Type I or a definite Carcinogen by the World Health Organization International Agency for Research on Cancer . However, the underlying pathogenic mechanisms on the molecular level, by which H.pylori causes inflammation and tumor, are poorly defined. Increasing data have shown that H.pylori infection causes inflammatory and immune responses in infected gastric mucosas, and that the imbalance between proliferation and apoptosis of the gastric mucosal cells caused by inflammatory responses is the important mechanism of gastric adenocarcinoma. NF-κB is the generic name of a family of transcription factors that play a critical role in immune, inflammatory and anti-apoptotic responses. Under no stimulatory conditions, NF-κB locates in the cytoplasm, combines with IκB , as a compound form, and its activation is suppressed by IκB. However when there are external signals of stimulation, IκB becomes phosphorylated by IκB kinase (IKK) complex. IκB separates from NF-κB, disengages its suppression of NF-κB, and the activated NF-κB is then released and translocated to the nucleus, where NF-κB activates its target genes by binding to specific sites in their regulatory regions.It has been repoted that H.pylori infection induces NF-κB activation, and NF-κB intercepts the activation of caspase 8 by...