摘要
背景与目的:研究幽门螺杆菌L型(helicobacter pyloriL-form,Hp-L型)抑制胃癌细胞BGC-823凋亡的作用及其作用机制。材料与方法:将BGC-823细胞与Hp-L型以不同比例(1∶20、1∶100、1∶500)共培养,以不加Hp-L型为对照组,在不同时段进行以下实验:倒置显微镜观察细胞形态学变化;透射电镜观察细胞凋亡及超微结构变化;流式细胞仪检测细胞凋亡率;免疫组化(SP法)检测细胞中凋亡抑制基因Livin、bcl-2及抑癌基因p53的表达情况。结果:与对照组相比,Hp-L型作用BGC-823细胞后,倒置显微镜观察到BGC-823细胞增殖旺盛,瘤巨细胞增多,并出现明显的凋亡抑制现象;电镜观察到BGC-823细胞凋亡形态特征及凋亡数目减少;流式细胞仪检测结果显示Hp-L型可降低BGC-823细胞的凋亡率(P<0.05);免疫组化结果发现BGC-823细胞中Livin、bcl-2和p53蛋白表达阳性率逐渐增加(P<0.05);以上作用均呈细菌浓度和作用时间依赖性(P均<0.05)。结论:Hp-L型可抑制胃癌细胞BGC-823凋亡,其机制与上调Livin、bcl-2、p53蛋白的表达有关。
BACKGROUND AND AIM：To investigate the effects of helicobacter pylori L-form（Hp-L）on apoptosis of gastric cancer cells BGC-823 and the probable mechanisms involved.MATERIALS AND METHODS：The BGC-823 cells were co-incubated with Hp-L in different ratios（1∶20,1∶100,1∶500）and the followings were carried out at different time points：morphology changes of BGC-823 cells were examined by inversion microscope;the ultrastructure of cells and the apoptotic morphology by transmission electronic microscopy;the apoptotic rate by flow cytometry and immunohistochemical staining（SP method）to detect the expression of Livin,bcl-2 and p53 in BGC-823 cells.RESULTS：When BGC-823 cells were infected by Hp-L,the cells proliferated well,many tumor giant cells appeared indicating obvious inhibition of apoptosis.The number of apoptotic cells and the apoptotic rate were both reduced.The expressions of Livin,bcl-2 and p53 were all increased.All the effects were in a concentration-and time-dependent manner.CONCLUSION：Hp-L could inhibit the apoptosis of gastric cancer BGC-823 cells,its mechanisms might be related to up-regulation of Livin,bcl-2 and p53 expressions.
出处
《癌变．畸变．突变》
CAS
CSCD
2009年第2期93-97,共5页
Carcinogenesis,Teratogenesis & Mutagenesis
基金
安徽省教育厅高校自然科学研究重点项目(KJ2007A098)
蚌埠市科技局2007年第一批科技项目(11)
