Methods: Mongolian Gerbils were challenged with or without H.pylori, and H.pylori colonization histopathology in the stomach were assessed by histological observation at six and twelve months post-challenge. DNA-PKcs and Ku70/80 expression were analyzed by immunohistochemistry. Results: At six and twelve months post-challenge,
there’s an increasing severity of IM (7/79). In addition, Ku expression was significantly lower in the infected gerbils than in the controls (p < 0.05, Studengt's t test). However, the expression of DNA-PKcs at six and twelve months infected gerbils increased without statistical find protocol difference (p > 0.05, Studengt’s t test). Post-immunisation gastritis was not associated with the expression levels of these two key repair factors. Conclusion: The H.pylori related IM gerbil model is the most extreme example of this type of pathology. This research demonstrated the potential function of H.pylori infection that may disturb the Ku stimulated signaling pathway of non-homologous end joining repair, thus trend to induce apotosis, genome instability and malignant pathological changes in gastric mucosa. Key Word(s): 1. Helicobacter pylori; 2. DNA-PKcs;
3. DNA damage repair; 4. Ku 70/80; Presenting Author: WEI LI Additional Authors: HUANONG LU Corresponding Author: WEI LI Affiliations: the First Affiliated Hospital of NanChang University Objective: Non-homologous selleck compound end joining (NHEJ) repair Cell Cycle inhibitor is a major but error-prone repair mechannism when cell suffer severe DNA damage, its key promoter is catalytic sunbunit of the DNA-dependent pro-tein kinase (DNA-PKcs) and Ku70/80 heterodimer. The pathology of gastric carcinoma is complicated and multifactorial, it’s also characterized by genomic instability, whereas the exact pathological mechanism is still unknown. The present study was undertaken to determine possible pathological role of DNA-PKcs and Ku70/80 mediating DNA repair
pathways in human gastric carcinoma tissues, as well as to verify whether H.pylori infection will disturb the regular repair function of gastric mucosa epithelial cells through a series of DNA damage response and non-homologous end joining repair pathway, thus lead to apotosis, genome instability and malignant pathological changes. Methods: Expression of DNA-PKcs and Ku70/80 were analyzed by immunohistochemistry in biopsies or surgical specimens of 180 patients with or without gastric carcinoma collected from January 2007 to September 2009 at the First Affiliated Hospital of Nanchang University. The specimens included 146 cases of gastric carcinoma specimen (GC) and 34 cases of normal gastric mucosa (NGM) as control.