Effect Of Helicobacter Pylori Infection On The Expression Of GST-Ï€ And P53 Protein In Intestinal Metaplasia

Carcinogenesis of gastric mucosa is a complicated pathological process including multiple steps and stages; meanwhile, a process of diversified pathological characteristics and lesions which can change one after another. In 1992, Correa summarized the pattern of gastric carcinoma progress, that is:"normal gastric mucosa→superficial gastritis→atrophy gastritis→intestinal metaplasia→dysplasia→gastric cancer"according to plenty of clinical materials and pathological data. Intestinal metaplasia of gastric mucosa(IM) is an adaptable pathological process which the normal gastric mucosa changes into intestinal epithelium and gland under the injurious stimuli. IM is a key process and an important precancerous lesion during the development of gastric cancer. Recently, many epidemiological and histological studies have suggested that the infection of Helicobacter pylori (H.pylori) is one of the most rates of important factors which induce gastric cancer and IM. It is very pity that the carcinogenesis of H.pylori have not elucidated, although the relationship has been confirmed widely between the H.pylori and gastric cancer.Therefore, it is very important significance to investigate the changing of gene and protein in the stage of IM, which is the important starting points during the gastric carcinogenesis, and to deeply understand the relationship between the H.pylori carcinogenesis.Glutathione S-transferase-π(GST-π) is an important protective material in our body, which has the role of anti-carcinoma and detoxification. Many researches showed that many extra cellular inducers and injured stimuli can make the abnormal expression of GST-πof gastric mucosa cells, accordingly remove the toxicity from the gene toxic substance in cytoplasm, protect DNA from injurous stimuli and maintain the steady of genetic materials and cellular normal function. To some extent, the changing of GST-πexpression can reflect the conditions of cellular function. Until now, p53 is a broadly researched anti-oncogene. Mutant p53 has close relationship with more than 50% tumor types including the gastric cancer, which is an important molecular event in human malignancies. There are two types of p53 gene, wild-type and mutant type. The wild-type plays the role of suppression, and the later plays the role of oncogene. The half-life period of mutant-type p53 is much longer, which can be detected by immunohistochemical method.Based on the above facts and problems, we would detect the expression of GST-πand p53 protein using the immunohisto chemical method, ELISA and trigeminy drug treatment in 30 cases normal gastric mucosa, 86 cases H.pylori-positive IM group, 96 cases H.pylori-negetive IM group, 45 cases eradication and no eradication IM groups, and 30 cases gastric cancers, to discuss the effect of H.pylori infection on the expression of GST-πand p53 protein, to understand roles of GST-πas a protect factors and p53 gene during the development of gastric caner, in order to reveal the relationship of H.pylori and gastric cancer. The results were as followed:(1) There was no expression of GST-πin normal gastric mucosa; the expression of GST-πin H.pylori-negative group was significantly higher than normal gastric mucosa group and gastric cancer group(P<0.01); The expression of GST-πin gastric cancer group is also obviously higher than normal gastric mucosa(P < 0.01). It is suggested that the protective role has been activated from normal gastric mucosa to IM stage, before the formation of gastric cancer.(2) We confirmed further that the expression of H.pylori-positive IM group was significantly higher than normal gastric mucosa group(P < 0.01), but obviously lower than H.pylori-negetive IM group(P < 0.01); there was no significant difference between the gastric cancer group and H.pylori-positive IM group. After the eradication of H. pylori, the expression of GST-πsignificantly increased comparing to pre-eradication(P<0.05). And no statistical significance with H.pylori-negative group. The results indicated that H.pylori infection decreased the expression of GST-π, and may increase the risk of gastric cancer by decreasing the protective role of GST-π.(3) By detecting the expression of p53 by immunohistochemical methods, we found there was no expression normal gastric mucosa. The expression of p53 in H.pylori-positive group is significantly higher than that of H.pylori-negative group and normal gastric mucosa(P<0.01), and obviously lower than that of gastric cancer group(P<0.01). There was on statistical significance between the H.pylori-negative IM group and normal gastric mucosa. The expression of p53 in gastric cancer group was obviously higher than that of normal gastric mucosa group and H.pylori-negative IM(P<0.01).(4) After eradication of H.pylori, the expression of p53 obviously lower comparing to pre-eradication in H.pylori positive-group(P<0.05), and no statistical significace comparing with the H.pylori-negative IM. These results suggested that H.pylori infection can improve the expression of mutant p53 gene, the phenomenon begin in the stage of IM during the process concluding by Correa,"normal gastric mucosa→superficial gastritis→atrophy gastritis→intestinal metaplsia→dysplasia→gastric cancer".In summary, we concluded that H.pylori infection exerts important roles in the progression of gastric cancer by either decreasing the protective role of GST-πor increasing the expression of p53 gene. The mechanism need to confirm by further research. In a word, H.pylori infection is an important factor of gastric cancer. It is realistic significance to decrease the accidence of gastric cancer by preventing the H.pylori infection, or eradication the infection of H.pylori early.