Observation of the changes of protein gene product 9.5, mucosal C-kit, gastrin and somatostatin in rat with experimental induced gastritis / 中国医师杂志

ABSTRACT

Objective To find the possible pathogenesis of enteric nervous system, gut hormone and gastric Cajal interstitial cell ( ICC ) in gastritis related gastrointestinal ( GI ) motor disorders on the changes of protein gene product 9. 5 in neurons , mucosal expression of C-kit, gastrin and somatostatin from the gastric wall of gastritis rat. Methods 45 rats were divided into 3 groups which included gastritis group A, gastritis group B and control group. Rats in gastritis group A were fed with Hp Sydney Strain 1, the mixture of 2% aspirin and 0. 6N hydrochloric acid was fed in gastritis group B. The control group only received saline. All of the rats were killed and mucosal tissue was obtained from antrum and greater curvature of the gastric body. Pathological and Hp examination were performed in the tissue slides, and then it was stained to check PGP 9. 5, gastric body's mucosal expression of C-kit, antrium's mucosal expression of gastrin and somatostatin. The cell body, the maximum diameter (Dmax, μm), mean area( μm2) and optical density (nm), integral optical density of the gastrin and somatostatin in the C-kit expression positive neurons from the gastric wall were compared among the groups. Result The mean area and optical density of PGP 9. 5 expression in neurons from the gastric wall of rat in group A or B were obviously lower than that of the control group ( P ＜0. 01 ), while there was no difference between gastric group A and B ( P ＞0. 05). Gastric group A had higher GAS expression than control group, while SS expression was lower than control group( P＜0. 05). There was no difference between group B and the control group in the two variances( P ＞0. 05).By linear correlation analysis, it showed that SS was negatively correlated with GAS ( r = - 0. 333, P ＜0. 01 ). The distributive area and diameter of cells with C-kit expression in both group A and B were significantly smaller than that in the control group ( P ＜ 0. 05 ), while there was no obvious difference between group A and B ( P ＞ 0. 05 ). There was no difference of integral optical density of the C-kit expression positive neurons among the three groups. Conclusions Hp infection and NSAIDs might cause gastritis and had influence on the structural changes of neurons from gastric wall and ICC. Hp infection could obviously inhibit SS excretion from antrum mucosa while increase Gastrin excretion. NSAIDs induced gastritis had little influence on GAS and SS.