摘要
目的:观察盐水灌胃导致大鼠萎缩性胃炎后胃黏膜组织病理变化及细胞超微结构变化,探讨长期咸饮食与慢性萎缩性胃炎发生的关系。方法:实验于2004-09/2005-07在西安市中心医院动物中心及解放军第四军医大学基础部电子显微镜中心完成。选择7周龄健康、性成熟的雄性SD大鼠64只,随机数字表法分为3组,即正常喂养组24只、灌胃对照组20只和盐水组20只。用盐水灌胃建立大鼠萎缩性胃炎动物模型。正常喂养组为正常喂养,饮凉白开水;灌胃对照组在正常喂养的基础上以25℃白开水灌胃,2.5mL/次,1次/d;盐水组在正常喂养的基础上以25℃150g/L盐水灌胃,2.5mL/次,1次/d。实验开始,先处死4只正常喂养组大鼠,并留取胃大体标本作为对照。以后各组分别于4,8,12,24,32周各抽取4只处死,光镜观察胃黏膜病理组织学改变,扫描电镜和透射电镜观察胃黏膜上皮细胞超微结构的变化。结果:纳入动物64只,均进入结果分析。①光镜见正常喂养组和灌胃对照组大鼠胃黏膜表面光滑,无糜烂,固有层无炎细胞浸润,黏膜下层无水肿,肌层无炎细胞浸润。盐水灌胃后第24周,大鼠胃黏膜出现腺体明显缩小,黏膜肌层的平滑肌呈束状增生插入黏膜固有层中。腺体上1/3至2/3腺上皮萎缩,腺管腔增宽,胃小凹颈部黏膜宽度变窄。②扫描电镜见正常喂养组和灌胃对照组大鼠胃黏膜被纵横交错的小沟分隔成许多胃小区,呈网状,胃小凹(胃腺开口)壁衬有圆形或椭圆形上皮细胞,体积基本一致,有短而稀的微绒毛。上皮细胞排列规则,被覆一薄层连续的黏液。盐水组大鼠在24周时胃黏膜表面扁平,腺细胞表面粗糙,腺腔间黏膜变宽,腺腔增大;并见局限性黏膜剥脱;到32周时,见胃黏膜上皮细胞萎缩、腺腔直径增大、细胞表面破溃,出现大小不等、形状不规则的糜烂面并见纤维性渗出。③透射电镜透见正常喂养组和灌胃对照组胃黏膜腺体饱满,腺腔完整,与周围连接紧密,腺细胞形态饱满,分泌颗粒丰富。盐水组24周,腺体萎缩,纤维结缔组织增生包绕腺体。腺细胞萎缩,胞质内细胞器减少,滑面内质网扩张,部分腺细胞代偿性增生,胞质内可见大量的线粒体,但细胞间距明显增大。盐水组32周,腺体萎缩更加明显,并可见少量细胞的核膜扩张,胞核常染色质减少,异染色质增多,靠近核膜,出现早期凋亡现象。结论:盐水灌胃可引起胃黏膜组织细胞损害,长期过咸刺激可损伤胃黏膜诱发黏膜萎缩。
AIM： To observe the tissue pathology and ultrastructural changes of gastric mucoea of experimental atrophic gastritis caused by salt-water in rats, and explore the relation between long-term salt diet and chronic atrophic gastritis. METHODS： The experiment was conducted from September 2004 to July 2005 in Animal Center of Xi＇an Municipal Central Hospital and Electron Microscopy Center of Basic Medicine School of Fourth Military Medical University of Chinese PLA. Totally 64 healthy mature male SD rats aged 7 weeks were divided into three group by table of random number. There were 24 rats in the normal feeding group, 20 rats in the normal control group and 20 rats in the salt-water group. The atrophic gastritis rat model was made by salt-water perfusion. The normal feeding group were gave normal feeding with plain boiled water; The normal control rats ware given plain boiled water in 25 ℃ perfusion with 2.5 mL every time and once a day; The salt-water group ware given 150 g/L salt water in 25 % perfusion with 2.5 mL every time and once a day. Four normal feeding rats were executed from the beginning and the gastric mucosa was preserved for normal control. With the progress of experiment, 4 rats from three groups were executed at weeks 4, 8, 12, 24 and 32, respectively. The pathology changes of gastric mucosa were observed under microscope and the ultrastructure of gastric mucosa was observed by scanning electron microscope and transmission electron microscope. RESULTS： Totally 64 included animals were involved in the result analysis. ①Under light microscope, in normal feeding group and normal control group, the surface of the gastric mucosa was smooth and no erosion. Inflammatory infiltration was absent in lamina propria. There was no edema in submucous layer and inflammatory infiltration in muscular layer. The gastric gland was shrunk obviously in salt-water perfusion grouP （salt-water was given for 24 weeks）. The smooth muscles in mucous muscle layer were hyperplasia and insert into lamina propria. The adeno- epithelium in the upper 1/3 to 2/3 edge of the gland was atrophic, the vessel became broaden and the width of rnucosa of gastric pit cervical part became narrow. ②Under scanning electron microscope, in normal feeding group and normal control group, the surface of gastric epithelium was lined regularly, mesh shape and was divided into many small section, and gastric fovea were covered with round or oval-shape epithelial cells in same volume with rare short tiny-villus. The epithelial ranged regularly and was covered by iaminar mucus; In salt-water perfusion group that the salt-water was given for 24 weeks, except for the surface of the gaStric mucosa became thin and fiat, the glandular cell became rough and the mucosa between two gastric gland and adeno-vessel were broaden it also could be seen limited exfoliation of mucosa; When the salt-water was given for 32 weeks, the gastric epithelial cells appeared shrunk, and the adeno-vessle was broaden and there was breakage in the Cell surface, Erosions of various sizes and shape and fibrous exudation could be seen there. ③The transmission electromicroscope observation： in normal feeding group and normal control group, the body of gland of gastric was chubby, adeno-vessel was integrity and bond tightly to milieu; glandular cell was also chubby and had a great deal secretary granule. In salt-water perfusion group that the salt-water was given for 24 weeks, except for the gastric gland was shrunk and connective tissue was hyperplasia to circle the gastric gland, glandular cell was atrophy, organell decreased and smooth endoplasrnic reticulum dilated. Parts of gland cell were compensatory hyperpiasia. There were a great deal of mitochondrion in the compensatory hyperplasia of glandular cell, but the distance between two cells was broadened clearly. When the salt- waterwas given for 32 weeks, glandular cell was atrophy distinctly and small nuclear membrane outspread. It also could be seen early apoptosis phenomenon： euchromatin decreased and heterochromatin increased near to nuclear membrane in small nucleus, CONCLUSION： Salt-water perfusion may cause the damage of the epithelia of gastric mucosa and long-term high-salt stimulation can induce the injury and evoke atrophy of gastric mucosa.
出处
《中国组织工程研究与临床康复》
CAS
CSCD
北大核心
2007年第4期703-706,I0003,共5页
Journal of Clinical Rehabilitative Tissue Engineering Research
基金
陕西省科技厅科研基金资助(2003K10-G68)~~
