丁酸钠诱导卵巢癌3AO细胞凋亡的研究

 目的　探讨丁酸钠 (NaB)诱导卵巢癌细胞株 3AO凋亡的机制。方法　以不同浓度的NaB对体外培养的 3AO细胞进行作用 ,通过光镜和DNA琼脂糖凝胶电泳观察凋亡发生与药物剂量和作用时间的关系 ,进而选取 4mmol/LNaB作用 72h的 3AO细胞为实验组 ,应用流式细胞技术分析Fas/FasL、bcl 2 /Bax表达和线粒体跨膜电位的变化 ,透射电镜观察内质网形态的变化。结果　 4mmol/LNaB作用72h ,光镜下可见 3AO细胞出现凋亡改变 ,DNA琼脂糖凝胶电泳中出现典型的DNAladder,线粒体跨膜电位降低 ,内质网肿胀 ,bcl 2表达降低 ,Bax表达升高 ,而Fas/FasL无明显改变。结论　NaB可能通过线粒体通路和内质网通路诱导 3AO细胞凋亡 ,bcl 2 /Bax起着重要的调控作用。

Study on Sodium Butyrate Induced Apoptosis in Ovarian Epithelial Carcinoma Cells 3AO

Objective To investigate the mechanism of sodium butyrate (NaB) induced apoptosis in ovarian carcinoma cells 3AO.Methods Human ovarian epithelial cancer 3AO cells were cultured in vitro and treated with NaB of different concentration for different time. Light microscopy and DNA ladder were applied to detect apoptosis. Then the expression of Fas/FasL and bcl-2/Bax,as well as the mitochondrion transmembrane potentials were analyzed through Flow Cytometry. Electron microscopy was performed to observe the changes of endoplasmic reticules.Results Being treated with NaB of 4mmol/L for 72 hours apoptosis appeared in 3AO cells. The morphologic characters of apoptotic cell were found by light microscopy,the characteristic DNA ladder turned out. The mitochondrion transmembrane potentials decreased;the endoplasmic reticulum swelled. There were up-regulation of Bax and down-regulation of bcl-2 but no dramatic changes in the expression of Fas and FasL. Conclusion Mitochondrion pathway and endoplasmic reticulum pathway probably involved in the mechanism of NaB induced apoptosis in 3AO cells. Bcl-2 and Bax played an important role in the procession.