Role of mitochondrial pathway in apoptosis of gastric cancer cell line SGC-7901 induced by Helicobacter pylori

张浩; 房殿春; 罗元辉; 兰春慧

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Role of mitochondrial pathway in apoptosis of gastric cancer cell line SGC-7901 induced by Helicobacter pylori

更新时间：2026-01-09

- Role of mitochondrial pathway in apoptosis of gastric cancer cell line SGC-7901 induced by Helicobacter pylori
- Journal of Army Medical University Vol. 31, Issue 5, Pages: 375-378(2009)
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  CLC： R377;R394.3;R735.2
- Published：2009
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张浩,房殿春,罗元辉,兰春慧.线粒体途径在幽门螺杆菌诱导胃癌细胞凋亡中的作用[J].陆军军医大学学报(原第三军医大学学报),2009,31(05):375-378.

　ZHANG Hao,FANG Dian-chun,LUO Yuan-hui,LAN Chun-hui.Role of mitochondrial pathway in apoptosis of gastric cancer cell line SGC-7901 induced by Helicobacter pylori[J].J Amry Med Univ (J Third Mil Med Univ),2009,31(05):375-378.
张浩,房殿春,罗元辉,兰春慧.线粒体途径在幽门螺杆菌诱导胃癌细胞凋亡中的作用[J].陆军军医大学学报(原第三军医大学学报),2009,31(05):375-378. DOI：

　ZHANG Hao,FANG Dian-chun,LUO Yuan-hui,LAN Chun-hui.Role of mitochondrial pathway in apoptosis of gastric cancer cell line SGC-7901 induced by Helicobacter pylori[J].J Amry Med Univ (J Third Mil Med Univ),2009,31(05):375-378. DOI：

摘要

目的探讨线粒体途径在幽门螺杆菌（H. pylori）诱导胃癌细胞凋亡中的作用。方法采用流式细胞术检测H. pylori NCTC 11637诱导的SGC-7901细胞凋亡，RT-PCR和Western blot法检测H. pylori感染对线粒体途径相关基因和蛋白表达的影响，并观察Caspase抑制剂对H. pylori所致SGC-7901细胞凋亡的影响。结果 H. pylori能够在体外直接诱导SGC-7901细胞凋亡，6、12、24 h和48 h的凋亡率分别为6.30%、11.57%、8.63%和7.22%；H. pylori能够呈时间依赖性地上调SGC-7901细胞的Bax蛋白表达，并促进Caspase-9和3的激活；Caspase-9和3抑制剂能够显著抑制NCTC 11637所致的SGC-7901凋亡，而Caspase-8抑制剂仅能部分抑制约20％NCTC 11637所致的SGC-7901凋亡。结论 H. pylori可引起SGC-7901细胞Bax基因和蛋白表达升高，激活Caspase-9和Caspase-3，且主要通过线粒体途径诱导细胞凋亡。

Abstract

Objective To evaluate the role of mitochondrial pathway in apoptosis of gastric cancer cell line SGC-7901 induced by Helicobacter pylori(H. pylori). Methods Apoptosis was evaluated in SGC-7901 cells by flow cytometry. RT-PCR and Western blotting were used to measure the expressions of genes and proteins associated with mitochondrial pathway. Effect of caspase inhibitors on apoptosis induced by H. pylori strain NCTC11637 was investigated. Results NCTC11637 directly induced apoptosis in SGC-7901 cells. Apoptotic rate was 6.30%

11.57%

8.63% and 7.22% respectively at 6

24 and 48 h after coculture with H. pylori. H. pylori upregulated the expression of Bax

and induced a time-dependent activation of caspase-9 and -3. Apoptosis was inhibited significantly by pre-incubation with the inhibitors of caspase-9 and -3. Caspase-8 inhibitor reduced H. pylori-induced apoptosis by 20%. Conclusion H. pylori infection upregulates the expressions of Bax mRNA and protein in gastric cancer cell line SGC-7901

and induces activation of caspase-9 and -3. Mitochondrial pathway may be the major one in H. pylori-induced apoptosis in SGC-7901.

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