大鼠实验性胃炎中PGP9．5、C—kit及胃泌素、生长抑素表达的观察研究

目的通过观察胃炎大鼠组织PGP9．5及c—kit与胃泌素（GAS）、生长抑素（SS）表达变化,探讨胃cajal间质细胞（ICC）、肠神经及胃肠激素在胃炎发病中的作用。方法45只大鼠分胃炎A组、胃炎B组、对照组3组,分别灌喂幽门螺杆菌（Hp）SS1菌株、2％阿司匹林和0．6N盐酸1：1混合液、生理盐水,处死后取胃窦及胃体组织PGP9．5染色及检测胃体黏膜C-kit及胃窦黏膜GAS、SS表达,测量胃壁神经元胞体、c—kit阳性表达的ICC最长直径（Dmax,μm）、平均面积（μm^2）及光密度（nm）以及GAS、SS表达的积分光密度,并进行比较。结果（1）胃炎A组、B组胃壁神经元表达PGP9．5细胞平均面积、光密度均低于对照组（P〈0．01）,胃炎A组与B组比较差异无统计学意义（P〉0．05）;（2）胃炎A组GAS表达明显高于对照组,而SS表达则低于对照组（P〈0．05）。胃炎B组与对照组比较两项表达结果差异均无统计学意义（P〉0．05）。直线相关分析显示SS与GAS呈负相关（r=-0．333,P〈0．01）;（3）胃炎A组、B组C-kit表达细胞分布面积和直径均明显小于对照组（P〈0．05）,胃炎A组与B组比较差异无统计学意义（P〉0．05）,三组c—kit表达细胞的积分光密度比较差异无统计学意义（P〉0．05）。结论Hp感染和NSAID可能改变胃壁神经元及ICC的形态结构。Hp感染可明显抑制胃窦SS分泌,而增加GAS分泌;NSAID诱导的胃炎对GAS与SS的影响不显著。

Observation of the changes of protein gene product 9.5, mucosal C-kit, gastrin and somatostatin in rat with experimental induced gastritis

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.