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目的探讨沙樱桃脂类对人胃癌MGC-803细胞的毒性作用及其机制。方法采用台盼蓝法检测细胞数、流式细胞仪检测细胞凋亡。将人MGC-803细胞分别与不同浓度的沙樱桃脂类(沙樱桃脂组)、5-FU(5-FU组)及PBS溶液(对照组)共同培养,观察沙樱桃脂类对人胃癌MGC-803细胞增殖的抑制作用。结果对人MGC-803细胞分别给予0.5、1.0、3.0mg/L沙樱桃脂类及10mg/L5-FU,培养6h、12h、18h、24h和48h,活细胞数随沙樱桃脂类浓度的增加和作用时间的延长而减少,与5-FU组相似(P>0.05),而与对照组比,差异有统计学意义(P<0.01);分析存活细胞率,表明人MGC-803细胞增殖被阻滞于G0G1期。在给予沙樱桃脂类0.5、1.0、3.0mg/L和5-FU培养48h后,人MGC-803细胞的凋亡率分别为13.8%、19.6%、26.2%和21.1%。结论沙樱桃脂类对人胃癌MGC-803细胞具有显著毒性作用,其机制可能与沙樱桃脂类可抑制MGC-803细胞分裂,并诱导其凋亡有关。
Objective To investigate the toxic effects and mechanisms of samara lipids on human gastric cancer MGC-803 cells. Methods Cell number was detected by trypan blue assay and apoptosis was detected by flow cytometry. The human MGC-803 cells were cultured with different concentrations of samara peach lipids (samara peach lipid group), 5-FU (5-FU group) and PBS solution (control group) -803 cell proliferation inhibition. The results showed that 0.5, 1.0 and 3.0 mg / L of sakurazalipids and 10 mg / L 5-FU were administered to human MGC-803 cells, respectively, and the number of viable cells increased with the concentration of saporin in 6h, 12h, 18h, 24h and 48h (P <0.05), while the difference was statistically significant (P <0.01); the survival cell rate was analyzed, indicating that the proliferation of human MGC-803 cells was increased by Blocked in G0G1 phase. The apoptotic rates of human MGC-803 cells were 13.8%, 19.6%, 26.2% and 21.1% respectively after the safflower lipids 0.5, 1.0, 3.0 mg / L and 5-FU were cultured for 48 h. Conclusion The sap flowering cherry juice has a significant toxic effect on human gastric cancer MGC-803 cells. The mechanism may be related to the inhibitory effect of samara cherry lipid on the cell division and induction of apoptosis in MGC-803 cells.