| The evidences from clinical and epidemiological studies show that H.pylori is the major etiological agent of chronic gastritis and peptic ulcer disease and is significantly associated with gastric carcinoma. The alteration of gastric epithelial cell turnover plays an important role in H.ylori associated gastritis. Recent evidences from studies to biopsy specimens have shown that H.pylori induces acceleration of apoptosis and proliferation in gastric epithelial cells; Apoptosis and proliferation decrease to normal level after eradication therapy；H.pylori and its excretion products can accelerate the cell turnover.Our study used proliferation cell nuclear antigen (PCNA) to evaluate the cell proliferation level. PCNA is also named cycle protein, an auxiliary factor of DNA polymerase δ. It's lowest expressed in Go phase, increases in late G1 phase, highest expressed in S phase, but declines in G2 and M phase. It's a mainly proliferation cell marker.Apoptosis is an important effect factor to the cell growth kinetics, playing an important role to sustain the cells normal quantity and function. It is initiative style to death different from necrosis, as the nuclear shrunk and broken, the apoptotic cell splits into several 'apoptosome' with membrane, can be engulfed by phagocyte. The character of this process is the chromatin resolves in control, DNA strands are broken at the spot of nucleosome joints, forming many 180-200bp fragments. Apoptotic cell can be detected by light microscope, electron microscope, or fluorescence microscope according to its morphology, by terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling(TUNEL) method to recognize 3′-OH bottoms, by gel electrophoresis to detect nucleosome DNA fragments, by flow cytometry and laser-scanning cytometor to do qualitative and quantitative analysis. The biopsy specimens' apoptosis are commonly used morphology methods to preliminarily test and confirmed by TUNEL. Our study detected hematoxylin-eosin stained tissues by light microscope and confirmed by TUNEL.The mechanism of H.pylori affecting the cell turnover is not clear. E2F-1 transcription factor is pivotal in control of cell proliferation and apoptosis, induces a coordinated expression of genes in G1 phase, initiate DNA synthesis, control the G1 to S transition of cell cycle. Overexpression of E2F-1 often leads to human tumors through deregulation the transition, it's reported that overexpression of E2F-1 lead to proliferation in the cell line BaF-B03, make the cell line not sensitivity to those cytokines which mediate apoptosis. The gene amplification and increased expression of E2F-1 were detected in human gastric and colorectal carcinoma, osteosarcoma and other cancer tissues. But a variety of experiments also showed that overexpression of E2F-1 mediated apoptosis through p53 dependent pathway or p53 independent pathway. It's important to investigate the expression of E2F-1 in H.pylori-infected gastric epithelial cell and examine the correlation between such expression and the cell proliferation and apoptosis to study further the etiopathology of H.pylori.It is considered widely that the gastric acid secretion determines the ending of H.pylori associated diseases. The pathogenic mechanism of H.pylori infection inducing duodenal ulcer (DU) distinguishes from gastric carcinoma. H.pylori infection mainly causes the antral inflammation in acid hypersecretion subjects, tends to induces DU. But in acid secretion having no change or decreased subjects, H.pylori infection tends to lead to atrophic gastritis with gastric body inflammation mainly, and furthermore leads to gastric carcinoma. But there were some reports recently of internal and external that duodenal ulcer patients proportion with gastric carcinoma at the same time, this is not consensus with conventional idea that the DU patients would not suffer from gastric carcinoma. Our study selected the chronic superficial gastritis and the DU patients with H.pylori infected, and to reflect the effects of... |
PDF Full Text Request