冬凌草甲素诱导乳腺癌Bcap37细胞凋亡的探索  

Exploration on Induction of Breast Cancer Bcap37 Apoptosis by Oridonin

作　　者：余越美 严巧灵[1] 章康健[1] 岳学田[1] 周秀梅[1] 

机构地区：[1]浙江理工大学生命科学学院新元医学与生物技术研究所,杭州310018

出　　处：《浙江理工大学学报（自然科学版）》2013年第3期377-382,共6页Journal of Zhejiang Sci-Tech University(Natural Sciences)

基　　金：浙江理工大学科研启动基金(1116818-Y)

摘　　要：探讨冬凌草甲素(oridonin)对人乳腺癌细胞Bcap-37的增殖、凋亡以及引起细胞凋亡机制。以不同浓度的Ori处理Bcap-37细胞,通过MTT法检测细胞生长抑制率;应用流式细胞分析术检测细胞凋亡;Western Blot检测细胞发生凋亡的机制。结果是48～96μmol/L的Ori可显著抑制Bcap-37细胞的增殖(P<0.05)。48μmol/L的Ori作用24h后,细胞的增值抑制率达到了40%,而96μmol/L的Ori只需处理12h,增值抑制率竟达到了50%。96μmol/L Ori处理24h后,Bcap-37细胞的凋亡率为21.6%。Western Blot检测到了Fas的上调,细胞色素c的释放和随后Caspase 9的激活及其下游信号蛋白Caspase 3和它的底物PARP,ICAD的剪切。进一步检测到Survivin的下调和GADD34的上调。基于这些实验结果,推测冬凌草甲素作为一种潜在的抗乳腺癌制剂,诱导乳腺癌细胞Bcap37发生凋亡的发生可能与Survivin和GADD34相关。This paper discusses the role of oridonin in the proliferation and apoptosis of breast cancer cell Bcap-37 and the mechanism causing apoptosis; treats Bcap-37 cell with Ori of different concentrations; detects cell growth inhibition rate with MTT method; detects apoptosis by using flow cytometry and the mechanism of apoptosis with Western blot. The result is that 48～96 μmol/L Ori can significantly inhibit the proliferation of Bcap-37 cell（P〈0.05）. After 24 h of operation of 48/,mol/L Ori, the proliferation in- hibition rate reaches 40%, while 96 tzmol/L Ori only needs 12 h treatment and the proliferation inhibition rate reaches 50%. After 24-hour treatment of 96 μmol/L Ori, the apoptosis rate of Bcap-37 cell is 21.6%. Western blot detects up-regulation of Fas, release of cytochrome c, activation of Caspase 9 and shear of its downstream signaling protein Caspase3 and its substrates PARP and ICAD. It further detects the downregulation of Survivin and up-regulation of GADD34. Based on these experimental results, it is inferred that the induction of apoptosis of breast cancer cell Bcap37 by oridonin as a potential anti-breast cancer preparation might be related to Survivin and GADD34.

关 键 词：冬凌草甲素 细胞凋亡 乳腺癌 CASPASE SURVIVIN GADD34 

分 类 号：Q789[生物学—分子生物学]