The Research On The Mechanism And The Expression Of Wei Shu Ling To Epidermal Growth Factor And Epidermal Growth Factor Receptor In Stomach Mucosa Of Chronic Gastritis Rats

Chronic gastritis has become the common and frequently encountered disease whichharms the digestive system of people at present. It refers to the pathological changes ofgastric mucosa caused by imbalance between the attack factors and the defense factorsthat is due to the destruction of the harmful factors. With the progress of the research onchronic gastritis, people have new understanding of its pathological mechanism. In theearly stage of chronic gastritis, parietal cells are damaged, gastric acid pH is increasedand gastric acid secretion is reduced, which caused the destruction of the mucus-HCO₃–barrier. It needs effective acid treatment. However with the worsening of pathologicalchanges in gastric mucosa, gastric gland will atrophy. Secretion of pepsin and innerfactors will correspondingly decrease. When the EGF and EGFR of gastric mucosa isalso destroyed, gastric mucosa atrophy irreversibly, glands disappear, and eventually itdeveloped into cancer of the stomach. Therefore the key factor in the treatment ofchronic gastritis is to reduce or eliminate the destruction of the attack factor andstrengthen the defensive factor.WSL is made of traditional Chinese medicine （TCM）such as the Artemisia argyi, Yuan hu,cuttlefish bone and so on. Previous studies foundthat WSL can improve EGF and EGFR expression, suggesting that WSL can improvegastric mucosal function. The purposes of the present study were to examine theprotective effect of WSL on experimental chronic gastritis in rats and to provide certainbasis for the rational application of WSL in treatment of chronic gastritis disease.Objective Investigate the effect of WSL on the expression in rats with chronic gastritismodel, and explore its role in gastric mucosa injury and possible mechanism of actionfrom the attack factor and defense factor two aspects.Methods Rats are randomly divided into normal control group, model control group,Wenweishu granules group, high and low doses group with WSL,20rats in each group. Experim-Ental gastritis is prepared in the later four groups by oral intake of sodiumsalicylate. The treatment for rats with WSL will take six weeks, and the weight changeof each mouse will be measured from zero weeks. The scope of hydrochloric acid,gastric juice pH value, the pathological changes in stomach tissue, electron microscopy,and the content of TGF-α、TXB₂and PGE₂in each mouse’s serum are also measured.COX₂、EGF and EGFR from stomach mucosal organization of chronic gastritis modelrats are measured by immunohistochemical.Results After the long-term administration of WSL to rats, the weight is obviouslyelevated, Gastric juice pH value and the activity of pepsin are decreased, the secretionof gastric juice volume, total acid secretion and total acidity are increased significantly.Gastritis pathological features of organization are improved. The activity of TGF-α andTXB₂in rats serum are decreased. The content of PGE₂is obviously enhanced. Whilethe content of EGF and EGFR in the gastric mucosa of model rats are obviouslydecreased.Conclusion WSL can effectively protect the gastric mucosa of chronic model rats, Theprotective mechanisms are reflected in the following two aspects: the first，WSL canreduce the secretion of gastric acid and pepsin. The second is that the protective factorEGF can improve the blood circulation in pathological changes of gastric mucosa,eliminate inflammation medium TGF-α、COX₂to stimulate the regeneration of gastricmucosa epithelial cell, and enhance PGE₂defense function of gastric mucosa. Itsmolecular mechanism of WSL may be related with the pathways of EGF／EGFR→TPK→Ras／Raf→MAPK.