胃癌和癌前病变患者细胞间隙连接改变与幽门螺杆菌感染的关系

目的:观察胃癌(gastric cancer,GC)和癌前病变(precancerous lesion,PL)患者胃上皮细胞间隙连接超微结构改变,探讨其与幽门螺杆菌(Helicobacter priori,H.pylori)感染的关系.方法:对70例GC,88例PL,33例慢性浅表性胃炎(chronic superficial gastritis,CSG)患者,进行快速尿素酶试验、碱性品红染色和14C尿素呼气实验以检测H.priori,聚合酶链式反应(polymerase chain reaction,PCR)法检测H.py-lorii CagA基因,并以透射电镜观察胃上皮细胞间隙连接超微结构改变.结果:PL患者胃上皮细胞单位周长连接长度小于CSG患者,细胞间隙最小宽度大于CSG患者.GC患者细胞连接数、单位周长连接数与单位周长连接长度小于CSG与PL患者,细胞间隙最小宽度大于CSG;CasA H.pylori感染者细胞连接数、单位周长连接数与单位周长连接长度均小于CagA-日.pylori感染者,细胞间隙最小宽度大于CasA-H.pylori感染者.PL患者H.pylori根除者胃上皮细胞间隙缩小,细胞连接长度增加,其单位周长连接长度大于未根除者,细胞间隙最小宽度小于未根除者.结论:GC和PL患者胃上皮细胞间隙连接改变与H.pylori感染,特别是与CagA H.pylori感染有关,H.pylori根除可促进细胞间隙连接形成.

Helicobacter pylori infection and changes of cell gap junction of gastric epithelial cells in patients with gastric cancer and precancerous lesion

OBJECTIVE: To observe the changes of cell gap junction ultrastructure of gastric epithelial cells in patients with gastric cancer(GC) and precancerous lesion(PL),and to investigate the relation between these changes and H.pylori infection. METHODS: Seventy patients with GC, 88 with PL, and 33 with chronic superfial gastritis (CSG) were studied. H.pylori was detected by rapid urease test,basic fuchsin stain and 14C-urea breath test. The CagA gene of H.pylori was determined by polymerase chain reaction(PCR).The cell gap junction ultrastructure was observed under transmission electronic microscope. RESULTS: Length of junction/unit perimeter of gastric epithelial cells in patients with PL was smaller than that in CSG patients, and the smallest width of the intercellular space was bigger than that in CSG patients. The number of cell junction, the number of junction/unit perimeter, and the length of junction/unit perimeter in patients with GC were all smaller than those in patients with CSG or PL, and its smallest width of the intercellular space was bigger than that in patients with CSG. In patients with GC, the number of cell junction, the number of junction/unit perimeter and the length of junction/unit perimeter in CagA+ H.pylori group were smaller than those in CagA(-) H.pylori group, and its smallest width of the intercellular space was bigger than that in CagA(-) H.pylori group. In PL patients, the intercellular space decreased, and the length of cell junction of gastric epithelial cells became bigger after H.pylori eradication. The length of junction/unit perimeter in patients of H.pylori eradication was bigger than that in patients without eradication, and the smallest width of the intercellular space was smaller than that in patients without eradication. CONCLUSION: The changes of cell gap junction of gastric epithelial cells in patients with GC and PL are associated with H.pylori infection especially CagA+ H.pylori infection. Eradication of H.pylori can promote the formation of cell junction.