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采用脂染素（ｌｉｐｏｆｅｃｔｉｎ）介导的ＤＮＡ 转染，Ｎｏｒｔｈｅｒｎ 印迹， ＭＴＴ和克隆形成实验，流式细胞术和细胞凋亡原位检测法探讨Ａｓ２Ｏ３ 对人宫颈癌ＳｉＨａ 和ＨｅＬａ 细胞的生物学效应和ｂｃｌ－２ 高表达对这一效应的影响． 结果表明，Ａｓ２Ｏ３ 处理的ＳｉＨａ 和ＨｅＬａ 细胞，存活率和克隆形成能力明显降低，细胞周期的Ｇ１ 期前有低于２ 倍体的凋亡峰，细胞被阻滞在Ｇ２／Ｍ 期，有细胞凋亡时出现的ＤＮＡ 断裂． 而Ａｓ２Ｏ３ 处理的ｂｃｌ－２ 高表达的ＳｉＨａ 和ＨｅＬａ 细胞存活率和克隆形成能力增加，凋亡率减少，Ｇ２／Ｍ 期阻滞程度显著降低． 结果表明，Ａｓ２Ｏ３ 可诱导ＳｉＨａ 和ＨｅＬａ 细胞凋亡，Ｇ２／Ｍ 期阻滞可能是其诱导凋亡的原因之一；ｂｃｌ－２ 高表达可能通过减轻Ｇ２／Ｍ 期阻滞的程度而部分阻止Ａｓ２Ｏ３ 诱导的细胞凋亡．
The biological effects of As2O3 on human cervical carcinoma SiHa and HeLa cells were investigated by lipofectin-mediated DNA transfection, Northern blotting, MTT and clonogenic assay, flow cytometry and in situ cell apoptosis detection Effect of bcl-2 overexpression on this effect. The results showed that the survival rate and clonogenic capacity of SiHa and HeLa cells treated with As 2 O 3 were significantly decreased. The apoptotic peak below 2-fold before G1 phase of the cell cycle was arrested, and cells were arrested in G2 / M phase. The DNA breaks when it dies. As2O3-treated bcl-2-overexpressed SiHa and HeLa cells increased their viability and colony-forming ability, decreased the apoptosis rate and significantly reduced the G2 / M phase arrest. The results showed that As2O3 can induce apoptosis of SiHa and HeLa cells, and G2 / M arrest may be one of the reasons for its induction of apoptosis. High expression of bcl-2 may partially prevent As2O3 by reducing G2 / M arrest Induced apoptosis.