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目的:探讨七叶皂苷钠诱导胃腺癌BGC-823细胞及胃癌AGS细胞凋亡的机制。方法:采用CCK-8法检测七叶皂苷钠作用后胃癌细胞活力的变化;倒置显微镜下观察胃癌细胞的形态变化;荧光倒置显微镜观察DAPI单染后细胞核形态的改变;流式细胞术检测细胞凋亡率;Western bloting检测JAK-1、STAT-1磷酸化情况;激光共聚焦显微镜观察STAT-1核转位情况。结果:七叶皂苷钠可浓度依赖性抑制胃癌细胞增殖,使胃癌细胞形态及细胞核形态呈现凋亡变化,显著升高癌细胞凋亡率,并下调JAK-1、STAT-1信号蛋白磷酸化及抑制STAT-1的核转位。结论:七叶皂苷钠能抑制BGC-823细胞及AGS细胞增殖并诱导其凋亡,该过程可能是通过抑制JAK-1/STAT-1信号级联来实现的。
AIM: To investigate the mechanism of sodium aescinate inducing gastric adenocarcinoma BGC-823 cells and gastric cancer AGS cell apoptosis. Methods: The changes of cell viability in gastric cancer cells treated with sodium aescinate were detected by CCK-8 assay. Morphological changes of gastric cancer cells were observed under inverted microscope. The morphological changes of nuclei were observed by fluorescence inverted microscopy. Cell apoptosis was detected by flow cytometry The rate of JAK-1 and STAT-1 phosphorylation was detected by Western bloting. The nuclear translocation of STAT-1 was observed by laser scanning confocal microscopy. Results: Sodium aescinate could inhibit the proliferation of gastric cancer cells in a concentration-dependent manner, which could induce apoptosis of gastric cancer cells in morphology and nuclear morphology, significantly increase the apoptosis rate of cancer cells and down-regulate the phosphorylation of JAK-1 and STAT-1 signaling proteins Inhibition of nuclear translocation of STAT-1. CONCLUSION: Sodium aescinate can inhibit the proliferation and induce the apoptosis of BGC-823 cells and AGS cells through the inhibition of JAK-1 / STAT-1 signaling cascade.