幽门螺杆菌急性感染对胃上皮细胞凋亡的影响  

Effects of acute Helicobacter pylori infection on apoptosis of gastric epithelial cells

作　　者：刘加霏 国东 褚衍六[3] 袁晓燕[2] 王明义 LIU Jiafei;GUO Dong;CHU Yanliu;YUAN Xiaoyan;WANG Mingyi(Department of Medical Laboratory,Weifang Medical University,Weifang,Shandong 261000,China;不详)

机构地区：[1]潍坊医学院医学检验学系,山东潍坊261000 [2]威海市立医院中心实验室,山东威海264200 [3]威海市立医院消化内科,山东威海264200

出　　处：《中国微生态学杂志》2020年第8期880-883,共4页Chinese Journal of Microecology

基　　金：威海市科技发展计划(2016GNS029);威海市医学微生物与免疫学重点实验室(2017GGH08)。

摘　　要：目的探讨幽门螺杆菌(Helicobacter pylori)急性感染对GES-1细胞凋亡的影响,揭示H.pylori引起GES-1细胞凋亡变化的分子机制。方法将H.pylori临床分离株SBK与胃上皮细胞GES-1按不同比例(感染复数MOI分别为50∶1和100∶1)共培养24 h,建立H.pylori急性感染模型。采用流式细胞仪分析GES-1的凋亡,通过Western Blot检测凋亡相关蛋白Bcl-xL、Bcl-2、Bax、Caspase-3和NF-κB p65的表达。经H.pylori感染的GES-1细胞为处理组细胞,未经H.pylori感染的GES-1细胞即为对照细胞。使用SPSS 21.0软件对结果进行统计学分析。结果GES-1细胞经H.pylori处理24 h后,与对照细胞相比,MOI为50∶1(t=11.040,P<0.001)和100∶1(t=6.936,P=0.002)的细胞凋亡率均明显增加;MOI为100∶1时GES-1细胞的凋亡率明显高于MOI为50∶1(t=4.875,P=0.008)。与对照组相比,处理组细胞的Bax、Caspase-3表达明显增高,NF-κB p65表达无明显变化,Bcl-xL和Bcl-2在MOI为50∶1时表达升高,而在100∶1时表达下调。结论H.pylori急性感染通过改变线粒体途径中凋亡相关蛋白Bax、Bcl-2及Bcl-xL的表达促进GES-1细胞凋亡,且GES-1细胞的凋亡程度与H.pylori的感染复数有关。Objective To investigate the effect of acute Helicobacter pylori infection on the apoptosis of GES-1 cells,and clarify the molecular mechanism.Methods Clinical H.pylori isolate SBK and GES-1 were co-cultured for 24 hours in different proportion(the MOI was 50∶1 and 100∶1 respectively).Apoptosis of GES-1 cells was analyzed by using flow cytometry.Expression of Bcl-xL,Bcl-2,Bax,NF-κB p65 and Caspase-3 were detected using Western Blot and the results were analyzed with SPSS 21.0 software.Results Compared with the control cells,the apoptosis rate of GES-1 cells increased significantly after 24 hours of H.pylori infection at MOI of 50∶1(t=11.040,P<0.001)and 100∶1(t=6.936,P=0.002).The apoptosis rate of GES-1 cells at MOI of 100∶1 was significantly higher than that of 50∶1(t=4.875,P=0.008).Compared with the control group,the expression of Bax and Caspase-3 were significantly upregulated in the treatment group;there was no significant change in the expression of NF-κB p65.The expression of Bcl-xL and Bcl-2 were upregulated at MOI of 50∶1,but downregulated at MOI of 100∶1.Conclusion Acute infection of H.pylori promotes the apoptosis of GES-1 cells by changing the expression of apoptosis related proteins Bax,Bcl-2 and Bcl-xL in the mitochondrial pathway,and the degree of apoptosis of GES-1 cell is related to the infection concentration of H.pylori.

关 键 词：幽门螺杆菌 胃上皮细胞GES-1 急性感染 凋亡 

分 类 号：R378.99[医药卫生—病原生物学]