| Objective:Chronic atrophic gastritis (CAG) is a refractory disease of digestive system diseases, which's main pathological changes including gastric mucosa and gastric glands thinning, lamina muscularis mucosae thickening, intestinal metaplasia, etc. Due to the atrophy of the gastric glandular organ, the gastric mucosa is thinner, together with intestinal metaplasia, inflammatory reaction and atypical hyperplasia. The clinical symptoms are including dyspepsia, epigastric discomfort or dull pain and anemia.CAG is a commonly encountered disease and frequently encountered disease of digestive system, characteristic with recurrent attacks. The disease rate rise with the age increase, soit is higher in the aged. Chronic superficial gastritis could develop to CAG. Because of relating to the gastric cance, CAG was classified as precancerous disease or precancerous disease by the WHO in 1978. According to the linkage theory of gastric cancer carcinogenesis, the pathological changes of gastric cancer carcinogenesis follow the step from chronic superficial gastritis (CSG), chronic atrophic gastritis (CAG), intestinal metaplasia, atypical hyperplasia and the end to gastric cancer. CAG as a kind of lesion precancerous has been generally accepted. The incidence of CAG is very high in China, and about 8% will develop to gastric cancer after 10 to 20 years. So discerning and preventing the precancerous disease and lesion precancerous of s digestive system as early as possible, are effective methods to decrease the incidence rate and death rate of gastric cancer.Gastrin is a kind of important gastrointestinal hormone, secreted by G cells. Gastrin affects the most functions of the gastrointestinal tract, promoting gastrointestinal secretion, promoting gastrointestinal movement, loosening pyloric sphincter and sphincter of Oddi and ileocecal junction, promoting gastrointestinal mucous cell division growth, promoting releasing trypsin and calcitonin.Motilin is a kind of straight chain polypeptides gastrointestinal hormone, constitute by 22 amino-acid residue. Motilin is secreted by Mo cells in the duodenum and proximate jejunal mucous membrane cryptae. Motilin directly affect to the acceptor of enteron smooth muscle cell, inducing smooth muscle contraction. Motilin secretes periodicity in interdigestive phase. The level of motilin in the digestive tract cancer patients is higher than health persons, and the mechanisms are indefinite.Gastritis I is an effective prescription which was found by Professor Liu Youzhang in his several decade clinical practices It has the effectiveness of strengthening spleen, benefiting vital energy, nourishing blood, regulating stomach and promoting granulation, and has been confirmed it's effectiveness in reconditioning gastric mucosa and resisting epithelial metaplasia of CAG. The purpose of our empirical study is to lucubrate the mechanism of gastritis I curing the CAG rats by lucubrating the mechanism of gastritis I regulating to serum gastrin and blood plasma motilin in stomach of the CAG rats, and to provide scientific experimental evidence of the clinical therapeutic effect of gastritis I.Methods:Our research was divided into overview and empirical study. We expounded the etiological factor, pathogenesis and therapeutic principle of ancient and contemporary doctor of TCM. We also expounded the advancement of modern medicine. In the empirical study,84 healthy SD rats were divided into 6 groups, including model group (24), normal group (12), western medicine control group (12), and 3 Gastritis I treatment group including high dose group (12), medium dose group (12), low-dose group (12). the CAG model rats was constructed by freely drinking the MNNG solution (50μg/ml), being intragastric administration and irregular diet. After the CAG model was constructed successfully, giving 5g/(kg·d) Gastritis I to high dose treatment group, giving 2.5g/(kg·d) Gastritis I to medium dose group, giving 1.25g/(kg·d) Gastritis I to low-dose group, giving 0.86 g/(kg·d) Wei Mei Su Pian to western medicine control group, the normal group was feed normally. We adopted radio-immunity echnology to detect the level of serum gastrin and blood plasma motilin.Result:①Our empirical study indicated that the method adopted to copy the CAG rats animal models was success. But the pathological changes were not typical enough, and persistence time was too long, the death rate was high, and the reductant MNNG is a kind of carcinogen, harm to the experimenter and the environment. Accordingly, our experiment program had successful, but not excellent enough.②The results of the serum gastrin level analysised by analysis of variance found that the serum gastrin level of the CAG model group rats was lower than normal control group (P<0.05). After treated by gastritis I, the curative effect of high and medium dose were better than low dose and Wei Mei Su Pian (P<0.05).③The results of the blood plasma motilin level analysised by analysis of variance found that the blood plasma motilin level of the CAG model group rats was higher than normal control group (P<0.01). After treated by gastritis I, the curative effect of medium dose was better than other groups (P<0.05).Conclusion:Our experiment had study the mechanism of gastritis I regulating to the serum gastrin and blood plasma motilin of the CAG rats by empirical study. The experimental results indicated:①Our study adopted synthetic methods to construct the CAG model rats. Those methods were able to build the CAG model rats successfully;②Gastritis I could improve the gastric mucosal lesion of the CAG rats;③The results of the serum gastrin level analysised by analysis of variance found that the serum gastrin level of the CAG model group rats was lower than normal control group. After treated by Gastritis I, the serum gastrin level of the CAG model group rats was rising.④The results of the blood plasma motilin level analysised by analysis of variance found that the blood plasma motilin level of the CAG model group rats was higher than normal control group. After treated by Gastritis I, the blood plasma motilin level of the CAG model group rats was decreasing.Gastritis I could improve the gastric mucosa damage of the CAG rats, and promote gastric mucosa plerosis, by raising the serum gastrin level and decreasing the blood plasma motilin level.
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