摘要
目的:研究雷公藤甲素诱导正常人肝细胞株L-02细胞凋亡的机制。方法:体外培养L-02细胞。MTT法检测雷公藤甲素的细胞毒性作用;Annexin V-FITC/PI双染法检测雷公藤甲素对L-02细胞的凋亡诱导作用;测定细胞基质中半胱天冬氨酸酶(Caspase)8、Caspase9与Caspase3活性的变化及加入Caspase抑制剂Z-DEVD-FMK后对细胞凋亡的影响。结果:雷公藤甲素能显著诱导L-02细胞的凋亡,其作用呈明显的量效关系与时间依赖性;120nmol·L-1雷公藤甲素作用L-02细胞24h使Caspase3的活性显著增强;加入Z-DEVD-FMK后,能有效抑制雷公藤甲素诱导的细胞凋亡。结论:雷公藤甲素体外诱导正常人肝细胞株L-02细胞凋亡可能与上调Caspase3、9的活性有关。
OBJECTIVE：To investigate the mechanism of triptolide-induced human liver cell L-02 apoptosis.METHODS：L-02 cells were cultured in vitro and the cytotoxic effects of triptolide were detected by MTT.Cell apoptosis was determined by FCM using the Annexin V-FITC/PI kit.The activity of Caspase 8,Caspase 9 and Caspase 3 were detected before and after incubated with the Caspase inhibitor.RESULTS：Triptolide markedly promoted L-02 cell apoptosis,positively correlated with the concentration of triptolide and the time.The activity of Caspase 3 increased significantly after L-02 cells treated with 120 nmol·L-1 triptolide for 24 h,and the addition of Z-DEVP-FMK effectively inhibited the apoptosis of L-02 cells.CONCLUSIONS：Triptolide induce apoptosis of human liver cell L-02,which is associated with the up-regulation of caspase 3 and caspase 9 activities.
出处
《中国药房》
CAS
CSCD
2012年第43期4036-4038,共3页
China Pharmacy
基金
财政部行业科研专项(中药毒性的评价方法学研究和科学应用)资助课题(200707008)
湖南省科技厅科技计划项目(2009FJ3027)
