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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.pyloriNCTC 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。
Objective To investigate the role of mitochondrial pathway in the induction of gastric cancer cell apoptosis by H. pylori. Methods Flow cytometry was used to detect the apoptosis of SGC-7901 cells induced by H.pylori NCTC 11637. The effects of H.pylori infection on the expression of mitochondria-related genes and proteins were detected by RT-PCR and Western blot. The effects of Caspase inhibitor on H Effect of pylori on apoptosis of SGC-7901 cells. Results H.pylori could directly induce the apoptosis of SGC-7901 cells in vitro. The apoptotic rate of SGC-7901 cells was 6.30%, 11.57%, 8.63% and 7.22% at 6, 12, 24 h and 48 h, respectively. Upregulate the expression of Bax in SGC-7901 cells and promote the activation of Caspase-9 and 3; Caspase-9 and 3 inhibitors can significantly inhibit the apoptosis of SGC-7901 induced by NCTC 11637, while Caspase-8 inhibitor It can partially inhibit the apoptosis of SGC-7901 induced by about 20% NCTC 11637. Conclusion H.pylori can induce the expression of Bax gene and protein in SGC-7901 cells, activate Caspase-9 and Caspase-3, and induce apoptosis mainly through the mitochondrial pathway.