三氧化二砷对人肺腺癌细胞株增殖和凋亡的影响

目的 研究三氧化二砷(As_2O_3)对人肺腺癌细胞株AGZY-83-a的抑制作用,探讨As_2O_3诱导人肺腺癌细胞株凋亡的机制.方法 采用MTT法、透射电镜及激光扫描共聚焦(LSCM)等方法 观察As_2O_3对人肺腺癌细胞株AGZY-83-a的影响.结果 As_2O_3能抑制人肺腺癌细胞株AGZY-83-a的生长,呈剂量依赖关系(P<0.01),IC_(50)=9.38μmoL/L;在光学显微镜及电镜下,可见As_2O_3,作用后的人肺腺癌细胞株AGZY-83-a呈现早期凋亡的变化特征:表面绒毛脱火,染色质块状散于核内;LSCM显示,As_2O_3,作用后人肺腺癌细胞株AGZY-83-a细胞内游离钙浓度(Ca~(2+)]_i)显著升高(P<0.01),呈剂量时间依赖关系.结论 As_2O_3能明显抑制人肺腺癌细胞株AGZY-83-a细胞的生长,并诱导人肺腺癌细胞株AGZY-83-a细胞凋亡,细胞内Ca~(2+)]升高可能是诱导细胞凋亡的机制之一.

Effects of arsenic trioxide on proliferation and apoptosis of human pulmonary adenocarcinoma

Objective To observe the pharmacological effects of arsenic trioxide(As_2O_3)on human pulmonary adenocarcinoma AGZY-83-a cells,and try to explore its mechanisms.Methods Inhibition percentage was detected by MTT assay;apoptosis was examined by transmission electron microscope and intracellular calcium concentration was investigated by laser scanning confoeal microscope(LSCM)in human pulmonary adenocarcinoma AGZY-83-a cells.Results As_2O_3 inhibited the proliferation of AGZY83-a in dose-dependent manner(P<0.01),the IC_(50) was 9.38 μmol/L;The early and media phase of apoptosis was observed:Surfacial floss break away and chromatomsome fragments scattered within neuclei;LSCM revealed that the concentration of intracellular calcium was elevated significantly after the treatment with As_2O_3 for 24 h、48 h、72 h(P<0.01)and showed relationship of concentration-time-dependent.Conclusion As_2O_3 can inhibit the proliferation of the AGZY-83-a cells and induce apoptisis of human pulmonary adenocarcinoma inoma AGZY-83-a cells,the increase of the intracellular calcium concentration may be one of its mechanisms.