| Infection of Helicobactor pylori is the main cause of chronic active gastritis (CAG), either is the significant cause and promoter of two precancerous lesions chronic atrophic gastritis (CAG) with intestinal metaplasia (IM) and dysplasia (DYS). Many studies showed that infection of H pylori is strongly related to the early stage of the progression and aggressiveness of gastric carcinoma (GC). H pylori has been classified as class 1 carcinogen for gastric cancer by the International Agency for Research on Cancer in 1994. H pylori can be divided in to two types according to the vacuolating cytotoxin A(Vac A) and the cytotoxin associated antigen A (Cag A). And Cag A positive H pylori is regarded to be strongly related to peptic ulcer and GC. Recent studies showed that H pylori induced cyclooxygenase-2 (Cox-2) expression in human gastric mucosa. Cox is the rate-limiting enzyme that catalyze the formation of prostaglandins from arachidonic acid .There are two distinct cox enzymes, a constructive enzyme(cox-l) and an inducible form(cox-2). Cox-1 is thought to be a housekeeping gene with essentially constant levels of expression, and its metabolites(PGs) have important cell protective effects in gastrointestine. Whereas cox-2 can not be found in normal tissues and is induced by proinflammatory stimuli, tumor promotors,oncogenes and carcinogenes. Recent studys showed that cox-2 is strongly expressed in gastrointestinal tumors such as colorectal cancers and gastric cancer. And epidemiologicstudies showed that nonsteroidal anti-inflammatory drugs (NSAIDs) such as Asprin can reduce the incidence of colorectal cancer, presumably through inhibition of cox-2. In order to investigate the possible mechanism of gastric carcinogensis and search for a new way of precautions and therapy of gastric cancer, we studied the role of cox-2 expression caused by H pylori in gastric carcinoma.Materials and Methods: (1) 55 cases of gastric carcinoma patients underwent surgical resection, samples were taken from tumor site and paracancerous tissues and 70 case of patients underwent endoscopy. All tissues were fresh and fixed immediately in 4% paraformaldehyde (include 1/1000 DEPC). Collect patient's serum and preserve at the temperature of -20℃. (2) In situ hybridization was used to examine the expression of cox-2mRNA. (3) Rapid urease test, warthin-starry dyer and c 14-urea breath test were used to detect H pylori. (4) Dot immunogold filtration assay was used to detect H pylori-CagA-IgG antibody. (5)The data were analysized by software SPSS 10.0. x 2-test and Spearman correlation was used to compare difference between groups. A difference was considered significant if the P value was below 0.05.Results: 1. cox-2mRNA was strongly expressed in gastric carcinomal cells and was also observed in some interstitial cells and smooth mucosa fibril. There was a intermediate to high level expression in IM and DYS, while detectable in low level in CSG. The positive rates of cox-2mRNA were U.5%. 323%, 58.8%, 80% in CSG, EVL DYS and GC respectively. The positive rates increased with the deterioration of lesions and there were significant differences between every two groups (P <0.05).2. The positive rate of cox-2mRNA in the well differentiated GC was 93.5%. The positive rate of cox-2mRNA in the poor differentiated GC was 62.5%. Expression of cox-2mRNA in the well differentiated GC were significantly higher than that in poor differentiated GC(P <0.05).3. Sexes -, ages have no impact on the expression. The positive rate of cox-2mRNA in the group with lymph node metastasis was 90.5%. The positive rate of cox-2mRNA in the group without lymph node metastasis was 46.2%. Expression of cox-2mRNA expression in the group with lymph node metastasis were significantly higher than thatin the group without lymph node metastasis (P <0.05).4. The positive rates of cox-2mRNA were 21.7%, 53.3%, 66.7%, 84.4% in H pylori-positive CSG, IM, DYS, GC respectively, and 0, 12.5%, 54.5%, 82.6% in H pylori-negative groups. The positive rate...
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