摘要
目的检测慢性胃炎各阶段黏膜细胞凋亡状况,探讨细胞凋亡在慢性胃炎发展过程中的意义及慢性胃炎(CG)胃黏膜细胞凋亡与幽门螺杆菌(Helicobecterpylori)感染、炎症程度、炎症活动度之间的关系。方法用TUNEL法检测6例正常胃黏膜、54例慢性浅表性胃炎(CSG)及28例慢性萎缩性胃炎(CAG)患者胃黏膜上皮细胞凋亡状况,分析黏膜细胞凋亡与胃窦H.pylori感染、黏膜炎症程度及活动度的关系。结果凋亡指数(AI)CSG>CAG>正常胃黏膜(P<0.05),而且炎症黏膜凋亡细胞分布与正常有所不同;在CAG,AI在肠化区<非肠化区。正常、H.pylori(-)CG、H.pylori(+)CG凋亡指数(AI)依次升高,组间差异均显著;H.pylori(+)CGAI依炎症轻、中、重度上升,轻、重度之间差异显著;H.pylori(+)CGAI随炎症活动度无、轻、中、重依次升高,差异均显著。Hp(-)CG,AI随炎症程度依次升高,但差异未达显著性;而炎症活动者AI显著高于非活动者。结论细胞凋亡在CAG黏膜萎缩及肠化发生中起重要作用。CAG黏膜AI下降可能与胃癌发生有关;H.pylori是最重要的致胃黏膜细胞凋亡因子;黏膜急性炎症细胞浸润是CG黏膜细胞凋亡的重要介导因素;黏膜慢性炎症细胞浸润在H.pylori致凋亡过程中也起一定作用。
Objective To investigate the significance of antral epithelial cell apoptosis in each stage of chronic gastritis and to analyze the relationship between gastric epithelial apoptosis and Helicobacter pylori （ tip ） infection, severity of chronic inflammation and activity of inflammation in chronic antral gastritis. Methods tip infection was detected and severity and activity of inflammation were evaluated in the gastric antral mucosa from 6 normal controls, 54 patients with chronic superficial gastritis （CSG） and 28 patients with chronic atrophic gastritis （CAG）. Apoptotic cells were detected by TUNEL. Results Apoptosis index （AI） in CSG was significantly higher than that in CAG （ 16.5 ± 4.1 vs 11.3 ± 3.9, P 〈 0.01 ） and in CAG was significantly higher than that in normal controls （11.3 ± 3.9 vs 3.3 ± 2.8, P 〈 0.01 ）. Furthermore, the distribution of apoptotic cells in chronic gastritis was different from that in normal controls. AI in no-metaplastic areas was significantly higher than that in intestinal metaplastic areas of CAG. AI in CG mucosa was significantly higher than that in normal mucosa. And AI in tip （ ＋ ） CG was significantly higher than that in tip （ - ） CG. For tip （ ＋ ） CG, AI increased in accordance with the severity of mucosal inflammation （mild, moderate, severe）, but statistics significance was only found in the comparison between mild and severe group; and AI increased significantly in accordance with the increase in the grade of mucosa inflam- mation activity （inactive, mild, moderate and severe ）. For tip （ - ） CG, no significant difference in AI was found among groups with different grades of mucosal inflammation, but AI in active CG was significantly higher than that in inactive CG. Conclusion Apoptosis plays an important role in the development of CAG and the decrease of AI in atrophic mucosa may contribute to the development of gastric carcinoma. Mucosa epithelial apoptosis is increased in CG, and tip is the most important inducing factor. Polymorphonuclear infiltration is an important mediating factor in epithelial apoptosis in CG. tip may also induce apoptosis via chronic inflammatory cell infiltration.
出处
《胃肠病学和肝病学杂志》
CAS
2006年第6期568-571,共4页
Chinese Journal of Gastroenterology and Hepatology
关键词
慢性胃炎
胃黏膜
凋亡
幽门螺杆菌
Chronic gastritis
Gastric mucosa
Apoptosis
Helicobacter pylori
