幽门螺杆菌感染与胃上皮细胞间隙连接功能的体外研究

目的　探讨幽门螺杆菌(H.pylon,Hp)对胃上皮细胞间隙连接通讯(GJIC)功能的影响及其发病机制。方法　应用Hp(包括Cag A 和Cag A-株)全菌和超声粉碎上清分别作用胃上皮细胞株SGC- 790 1。采用激光扫描共焦显微镜(L SCM,L eica TCS SP)以荧光光漂白后再恢复(FRAP)技术测定SGC- 790 1细胞GJIC功能(以荧光传递速率K表示,×10 - 3/ s)。结果　Cag A 和Cag A- Hp株均下调SGC- 790 1细胞GJIC功能(Cag A :F=5 7.98;Ca-g A- :F=2 9.5 9,P<0 .0 1) ;且Cag A 与Cag A- Hp相比前者更显著下调胃上皮细胞GJIC功能(全菌:t=13.86 ,P<0 .0 1;超声粉碎上清:t=11.87,P<0 .0 1)。结论　Cag A 比Cag A- Hp显著抑制胃上皮细胞的GJIC功能,提示其在胃癌发生中起重要作用。

Relationship between helicobacter pylori infection and gap junction function of gastric epithelial cells in vitro

Objective To study the influence of Hel ic obacter pylori infection on GJIC and its mechanism. Methods A human gastric epithelial cell line (SGC-7901) was grown on coverslips,then expo sed overnight to (CagA or CagA- strain) H.pylori intact bacteria and s onicate extract,respectively.GJIC between those cells was determined using the f luorescence redistribution after photobleaching (FRAP) assay.Results When compared with control which cells were cultured in medium alone,both CagA and CagA- H.pylori isolates includi ng intact bacteria and sonicate extract could inhibit gap-junction function in SGC-7901 cells (CagA :F=57.98;CagA-:F=29.59,P<0.01).Compared w ith CagA- strain,CagA strain significantly down-regulated GJIC function o f gastric cells in vitro (the intact bacteria samples:t=13.86,P<0.0 1;the sonicate extract samples:t=11.87,P<0.01). Conclusions When compared with CagA- H.pylori,CagA H.pylori strain can d own-regulate the gap junction function significantly,which may play an importan t role in gastric carcinogenesis.