摘要
目的探讨熊去氧胆酸(UDCA)对肝肿瘤细胞株诱导凋亡及抑制增殖的作用和机制。方法用四氮唑蓝法、流式细胞术、脱氧核糖核苷酸末端转移酶介导的缺口末端标记法、Wright-Giemsa染色法、电镜及免疫细胞化学等方法,观察UDCA对肝肿瘤细胞株HepG2、BEL7402和正常人肝细胞株L-02的生长活力、细胞凋亡、细胞周期及Bax/bcl-2基因表达的影响。结果UDCA对HepG2、BEL7402细胞株具有显著地抑制生长、诱导凋亡、阻滞细胞周期于S期、降低bcl-2和提升Bax表达的作用。UDCA对HepG2及BEL7402的IC50分别为0.92,0.86mmol/L。UDCA(1.0mmol/L)对HepG2及BEL7402的凋亡率分别为42%及44%,明显高于对照组(P<0.01)。UDCA对L-02细胞无明显作用。结论UDCA对HepG2、BEL7402细胞株有显著地抑制增殖及诱导凋亡作用,该作用可能与UDCA阻滞细胞周期、降低bcl-2和提升Bax的表达有关。
Purpose To investigate the effect of inducing apoptosis and inhibiting proliferation on hepatoma cell lines by UDCA, and mechanisms of the action. Methods UDCA effect of cell proliferation, apoptosis, cell cycle and the expression of Bax/bcl-2 genes on two human hepatoma cell lines HepG2 and BEL7402, and normal human hepatic cell line L-02 in vitro was detected by MTT assay, flow eytometry, TUNEL assay, Wright-Giemsa staining, electron microscopy and immunoeytoehemistry. Results UDCA could strongly inhibit the proliferation, induce apoptosis, arrest cell cycle to S phase, down-regulate bel-2 and up-regulate Bax gene expression of HepG2 and BEL7402 cell lines. The IC50 to HepG2 and BEL7402 were 0.92,0.86 mmol/L, respectively. The apoptosis rates (UDCA/1.0mmol/L) of HepG2 and BEL7402 were 42% and 44%, respectively, the rates were significantly higher than those of L-02 (P 〈 0.01). UDCA had no obvious effect on L-02 cell line. Conclusion UDCA maybe selectively inhibits proliferation and induces apoptosis of HepG2 and BEL7402 cell lines by blocking cell cycle and regulating the expression of Bax/bel-2 genes.
出处
《中国生化药物杂志》
CAS
CSCD
2005年第4期199-202,共4页
Chinese Journal of Biochemical Pharmaceutics
关键词
熊去氧胆酸
肝肿瘤
细胞凋亡
细胞株
ursodeoxycholic acid
liver neoplasms
apoptosis
cell lines