摘要
目的 研究紫草素诱导人黑色素瘤A375 S2细胞凋亡的分子机制。方法 MTT法、Hoechst33258荧光染色、DNA片段化分析、Westernblot、流式细胞分析以及caspase活力分析等。结果 10μmol·L-1紫草素可明显地抑制A375 S2细胞的生长,其半数有效抑制浓度IC50为 (10 9±1 8)μmol·L-1。10μmol·L-1紫草素可诱导A375 S2细胞凋亡,并经历了caspase 9和caspase 3的激活。紫草素促进p53蛋白的积聚,Bax蛋白表达的上调和Bcl xL蛋白表达的下调,进而导致细胞色素C的释放,致使细胞凋亡。紫草素可使细胞周期停止在G1 期。结论 紫草素可诱导A375 S2细胞周期停止在G1 期,其诱导细胞凋亡的途径经过p53介导的Bax和caspase 9的激活。
Aim To study the mechanisms of shikonin-induced A375-S2 cell apoptosis. Methods Cytotoxicity assay by MTT, DNA fra gmentation assay, caspases activity assay, flow cytometric analysis and Western blot analysis were carried out. Results Shikonin markedly inhibite d A375-S2 cell growth. IC 50 of the 24 h time course was (10.9±1.8) μm ol·L -1. Apoptotic cell death was observed within 24 h after 10 μmol·L -1 shikonin treatment. Shikonin induced A375-S2 cell apoptosis involved in the activation of caspase-3 and caspase-9. Shikonin induced accumulation of p5 3 and up-regulation of Bax and down-regulation of Bcl-xL which are mediated b y p53, resulted in a release of cytochrome C. Shikonin arrested cell cycle at G 1 phase in A375-S2 cells. Conclusion Shikonin induced cell cycl e arrest at G 1 phase in A375-S2 cells, and induced A375-S2 cell apoptosis vi a activation of Bax and caspase-9 mediated by p53.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2005年第2期202-205,共4页
Chinese Pharmacological Bulletin
