摘要
目的：明确三氧化二砷对人肝癌细胞的诱导凋亡作用及其分子机制。方法：用四甲基偶氮唑蓝法、AO/EB荧光染色法、透射与扫描电镜观察、DNA电泳、流式细胞术、TUNEL法及免疫组织化学等方法，观察了三氧化二砷对体外培养的人肝癌细胞株QGY-7701、QGY-7703和正常人肝细胞株L-02的生长活力、细胞凋亡、细胞周期及其相关基因表达的影响。结果：三氧化二砷能显著地抑制人肝癌细胞QGY-7701和QGY-7703的生长，用药后诱导其出现了典型的细胞凋亡形态学和生化学改变，并使细胞周期阻滞于S期，且bcl-2基因表达明显下降，bax和Fas基因表达显著增强；三氧化二砷对正常人肝细胞株L-02无明显作用。结论：三氧化二砷对人肝癌细胞有显著的选择性诱导凋亡作用，且受到多种基因调控，这一结论为应用三氧化二砷治疗原发性肝癌提供了可靠的实验依据。
Objective: To study the possible apoptosis-inducing effect of arsenic trioxide on human hepatocarcinoma (HCC) cells, and its molecular mechanisms. Methods: Arsenic trioxide action on the cell growth, apoptosis, periodicity and the expression of related genes in two human hepatocarcinoma cell lines QGY-7701 and QGY-7703, and normal humanhepatic cell line L-02 in vitro was observed by MTT assay, acridine orange (AO) /ethidiumbromide (EB) fluorescent staining, electron microscopy detection, DNA gel electrophoresis, flow cytometry, TUNEL assay and immunohistochemical staining. Results: Arsenic trioxide could strongly inhibit the growth of human hepatocarcinoma cells QGY-7701 and QGY-7703 with the cell cycle arrested on S phase, and induce the apoptosis of the cells with bcl-2 gene expression down-regulated and bax and Fas gene expression up-regulated. But arsenic trioxide had no obvious effect on the normal hepatic cells. Conclusion: Arsenic trioxide has significant selective apoptosis-inducing effect on the human hepatocarcinoma cells, which is regulated by several genes. The results provide the credible experimental basis for clinically treating HCC with arsenic trioxide.
出处
《中华肝脏病杂志》
CAS
CSCD
2000年第6期367-369,共3页
Chinese Journal of Hepatology
基金
江苏省科委青年科技基金!(BQ98048)
关键词
肝细胞癌
三氧化二砷
细胞凋亡
Carcinoma, hepatocellular
Apoptosis
Gene
Arsenic trioxide
