三氧化二砷诱导人宫颈癌细胞凋亡及bcl-2高表达对其影响

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．

Arsenic trioxide induced human cervical cancer cell apoptosis and effect of bcl 2 overexpression on it

Lipofectin mediated DNA transfection, MTT reduction, clone forming assay, flowcytometric analysis and in situ cell death detection were used to study the biological effect of As 2O 3 on human cervical cancer SiHa and HeLa cells and the protection by bcl 2. The results showed that the survival and clone forming rate of SiHa and HeLa cells were decreased by treatment of As 2O 3. The cells showed hypodiploid peak before G 1 phase and were blocked in G 2/M phase as well as DNA fragmentation. Compared to their material cells, the survival rate of As 2O 3 treated SiHa and HeLa cells with bcl 2 overexpression was increased while apoptotic rate was decreased as well as the G 2/M arrest of the cells was partly reversed. The results suggest that As 2O 3 induces apoptosis of SiHa and HeLa cells possibly via inducing G 2/M arrest; overexpression of bcl 2 partly inhibits As 2O 3 induced apoptosis, which is related to prevent the cells from As 2O 3 caused G 2/M block.