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目的探讨三氧化二砷(As2O3)对SPCAⅠ/人肺腺癌细胞株的抗增殖效应及诱导细胞凋亡的作用。方法将SPCAⅠ/人肺腺癌细胞株培养传代,分别加入不同浓度的三氧化二砷,作用24小时后,分别以酶标仪检测细胞抑制率、FACSAr-ia流式细胞仪检测细胞凋亡率、倒置显微镜观察凋亡细胞形态。结果不同浓度的三氧化二砷体外对人肺腺癌细胞株SPCA/Ⅰ均有直接的抑制作用,其抑制率与所用药物浓度呈正相关;三氧化二砷体外对人肺腺癌细胞株SPCAⅠ/有诱导凋亡的作用,细胞凋亡率明显增加。倒置显微镜见细胞由原来贴壁生长而逐渐脱落、外形变圆、体积缩小、折光性增强,核染色质凝集,细胞裂解。结论三氧化二砷能通过诱导细胞凋亡,直接抑制人肺腺癌细胞株SPCAⅠ/增殖。
Objective To investigate the antiproliferative effect of arsenic trioxide (As2O3) on SPCAⅠ / human lung adenocarcinoma cell line and its effect on inducing apoptosis. Methods SPCAⅠ / human lung adenocarcinoma cell lines were cultured and passaged, and different concentrations of arsenic trioxide were added respectively. After 24 hours, the cell inhibitory rate was detected by microplate reader. The apoptosis rate was detected by FACSAr-ia flow cytometry. Observation of apoptotic cell morphology. Results Different concentrations of arsenic trioxide had a direct inhibitory effect on human lung adenocarcinoma cell line SPCA / Ⅰ in vitro, and the inhibition rate was positively correlated with the concentration of the drug used. The effect of arsenic trioxide on the apoptosis of human lung adenocarcinoma cell line SPCAⅠ / , Apoptosis rate increased significantly. Inverted microscope see the cells from the original adherent growth and gradually fall off, the appearance of round, reduced size, enhanced refraction, nuclear chromatin condensation, cell lysis. Conclusion Arsenic trioxide can directly inhibit human lung adenocarcinoma cell line SPCAⅠ / proliferation by inducing apoptosis.