【摘 要】
：
通过实验和临床观察幽门螺杆菌(Helicobacter pylori)对胃上皮细胞间隙连接超微结构的影响,从细胞间隙连接角度探讨H.pylori 致癌机制.将不同H.pylori 菌株与BGC-823细胞共培
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通过实验和临床观察幽门螺杆菌(Helicobacter pylori)对胃上皮细胞间隙连接超微结构的影响,从细胞间隙连接角度探讨H.pylori 致癌机制.将不同H.pylori 菌株与BGC-823细胞共培养24 h或48 h,用原位固定与原位包埋法透射电镜观察细胞间隙连接超微结构变化.对70例胃癌患者,用快速尿素酶试验、碱性品红染色和14℃尿素呼气实验检测H pylori,PCR法检测H.pylori CagA基因,及透射电镜观察胃上皮细胞间隙连接超微结构变化,结果显示,未加H.pylori 组BGC-823细胞可见较多细胞连接及连接复合体,加H .pylori 各组细胞的连接数、单位周长连接数与单位周长连接长度均小于未加H.pylori组,而细胞间隙最小宽度大于未加H.pylori组(P＜0.001或P＜0.005),且CagA+的NCTC J99组、临床株GC01组和NCTC11639组细胞连接数、单位周长连接数均小于CagA-的NCTC 12908组(P＜0.001或P＜0.05),NCTC J99组与临床株GC01组细胞单位周长连接长度短于NCTC 12908组(P＜0.001).胃癌患者H.pylori 感染组细胞连接数、单位周长连接数与单位周长连接长度均小于无H.pylori感染组,细胞间隙最小宽度大于无H.pylori感染组(P＜0.001),且CagA+ 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-H,pylori 感染者,细胞间隙最小宽度大于CagA- H.pylori 感染者,上述结果表明,胃上皮细胞间隙连接改变与H.pylori 感染,特别是CagA+ H.pylori感染有关.
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