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目的明确非甾体消炎药(NSAIDs)诱导胃癌细胞凋亡情况和不同p53基因表型对NSAIDs诱导细胞凋亡的影响。方法通过MTT比色法检测NSAIDs对细胞生长活力的影响;应用丫啶橙染色、Annexin-V/PI双染色、共聚焦显微镜、TUNEL法检测细胞凋亡;应用流式细胞术进行凋亡细胞计数。结果NSAIDs药物吲哚美辛(Indo)和阿斯匹林(Asp)对胃癌细胞株AGS(p53+/+)、MKN28(p53-/-)均有显著的生长抑制作用,且呈时间依赖性增强。一定浓度的NSAIDs作用一定时间后,AGS、MKN28细胞均发生凋亡的形态学和生化学改变。在相同作用条件下,AGS细胞凋亡率明显高于MKN28细胞。处理组MKN28细胞凋亡数量虽有所增多,但不具有统计学意义 结论NSAIDs可诱导胃癌细胞凋亡,AGS细胞对NSAIDs更为敏感,Indo的凋亡诱导作用更为强烈。p53基因突变可能阻断了NSAIDs绣导的细胞凋亡。
Objective To investigate the effects of non-steroidal anti-inflammatory drugs (NSAIDs) on the apoptosis of gastric cancer cells and on the apoptosis of NSAIDs induced by different p53 phenotypes. Methods MTT colorimetric assay was used to detect the effect of NSAIDs on cell viability. Apoptosis was detected by acridine orange staining, Annexin-V / PI double staining, confocal microscopy and TUNEL. Flow cytometry . Results NSAIDs Indo and Asp inhibited the growth of gastric cancer cell lines AGS (p53 + / +) and MKN28 (p53 - / -) in a time-dependent manner . A certain concentration of NSAIDs after a certain period of time, AGS, MKN28 cells were apoptotic morphological and biochemical changes. Under the same conditions, the apoptosis rate of AGS cells was significantly higher than that of MKN28 cells. Although the number of apoptotic MKN28 cells in the treated group increased, it was not statistically significant. Conclusion NSAIDs can induce apoptosis of gastric cancer cells, AGS cells are more sensitive to NSAIDs, Indo induced apoptosis is more intense. Mutations in p53 gene may block apoptosis of NSAIDs-embroidered cells.