The Mechanism Of Isinglass In Prevention And Treatment Of Chronic Atrophic Gastritis

Chronic Atrophic Gastritis (CAG) is a common disease in clinic. Because of its positive correlation with morbidity of gastric carcinoma, it was considered as a precancerous condition by World Health Organization (WHO). For this reason, to prevent and cure CAG plays a very important role in preventing gastric carcinoma. In this study, we reestablished an animal model of rats with CAG in accordance with the previous experience of combined administration of 60% ethanol, 20mmol/L sodium deoxycholate and 0.1% ammonia water. In one group, sucralfate and isinglass were used as preventive therapy while we were establishing CAG rat model. In the other group, sucralfate and isinglass were used to treat rats after establishment of CAG rat model. Then proliferation zone of gastric mucosa and serum growth factors level were measured in order to explore the mechanism of isinglass on CAG rats. To explore a new method of preventing and treating chronic atrophic gastritis is the ultimate aim of this study.Materials and Methods80 healtiiy, sexual mature, qualified female SD rats were tested, weighting 200+lOg, provided by Zhejiang Medical Institute. All the rats were randomly divided into 8 groups. The rats in Normal Control Group were raised in a routine way for 32 weeks. The rats in Model Control Group were administered with 60% ethanol, 20mmol/L sodium deoxycholate and 0.1% ammonia water for 24 weeks. Then they were fed in a routine way for 8 more weeks. Three groups of ratsunder prevention test were administered by isinglass 160mg/100g/d, 80mg/100/d and sucralfate 160mg/100g/d respectively in each morning for 24 weeks. Three groups of rats in reverse test were continuously administered by isinglass 160mg/100g/d, 80mg/100g/d and sucralfate 160mg/100g/d respectively in each morning for 8 more weeks after the CAG model was established. Then these rats were anaesthetized by 1% thiopental sodium in foodless condition. Sml/per blood were taken from carotid through catheter. The level of serum EGF and GH were measured by radioimmunoassay. Then their stomachs were removed. The gastric streak-like samples for histological examination were cut along their lesser curvature and greater curvature respectively. Then they were immediately immersed in 10% buffered formalin and embedded in the paraffin. Paraffin sections were cut, mounted on glass slides, stained with HE, and with immunohistochemistry for proliferating cell nuclear antigen (PCNA). The pathological pattern of gastric mucosa and the length of the proliferation zone from top to bottom of PCNA positive cells were observed.ResultsThe experimental results showed the CAG model was successfully established by administration of 60% ethanol, 20mmol/L sodium deoxycholate and 0.1 % ammonia water. HE slides revealed: mucosal glands reduced and arrayed disorderly. Mucosal muscle layer became thick. Plenty of Inflammatory cells immersed in gastric mucosa, partly congregated. No intestinal metaplasia and atypical hyperplasia were found.Pathological patterns of isinglass prevention groups were similar to that of normal control group. However pathological patterns of isinglass reverse group were much better than that of model control group, even close to that of normal control group. HE slides revealed: mucosal glands arrayed closely and regularly. Only a few of inflammatory cells were found.After preventive treatment with isinglass, the mean of length of antrum mucosa PCNA positive zone was 129.38um in high dose isinglass group, 125.50um in low dose isinglass group, which were very close to normal control group 123.29um (p>0.05). They were both much better than model control group 57.14um (p<0.01). The EGF level was 3.69ng/ml in high dose isinglass group, 4.04ng/ml in low dose isinglass group, both higher than normal control group 0.6Ing/ml(p<0.01) and model control group 2.24ng/ml (p<0.05). The GH level was 18.Ing/ml in high dose isinglass group, 17.47ng/ml in low dose isinglass group, both similar to normal control group 18.01ng/ml, and model control group 18.48ng...