摘要
目的:研究自兴安升麻提取的23-O-乙酰升麻醇-3-O-β-D-木糖苷对HepG2细胞的细胞毒性及其作用机制。方法:利用MTT法进行细胞毒活性测定;用AO/EB染色法观察细胞个体的凋亡;以流式细胞光度术研究细胞周期的改变并验证凋亡的产生;用蛋白印迹技术从分子水平阐明该化合物的细胞毒作用机制。结果:23-O-乙酰升麻醇-3-O--βD-木糖苷可以明显抑制HepG2细胞生长,IC50为16μmol.L-1。同时该化合物可以使HepG2细胞产生凋亡形态学变化和G2-M细胞周期阻滞,并使PARP蛋白裂解,bc l-2,Bax,cdc 2和cyc lin B等凋亡和细胞周期相关蛋白表达改变。结论:23-O-乙酰升麻醇-3-O--βD-木糖苷对HepG2细胞具有明显的细胞毒作用,该化合物可诱导HepG2细胞凋亡和G2-M周期阻滞,其凋亡机制涉及caspases家族激活,bc l-2和Bax表达改变,而G2-M周期阻滞与cdc 2和cyc lin B下调直接相关。
Objective： To elucidate the cytotoxicity and mechanism of 23-O-acetylcimigenol-3-O-β-D-xylopyranoside isolated from C. dahurica on HepG2 cells and to find the leading compound for new drug development. Method： MTT, AO/EB staining observation, flow cytometry and western blot methods were used to study the cytotoxicity, morphological changes, cell cycle distribution and protein expression profile of 23-O-acetylcimigenol-3-O-β-D-xylopyranoside on HepG2 cells. Result： 23-O-acetylcimigenol-3-O-β-D-xylopyranoside could inhibit the proliferation of HepG2 cells with IC50 at 16 μmol · L^-1 , and could also induce apoptosis and G2-M cell cycle arrest. Further study demonstrated that the compound could cleavage PARP, regulate protein expression of bcl-2 family and decrease the expression of cdc 2 and cyclin B. Conclusion： 23-O-acetylcimigenol-3-O-μ-D-xylopyranoside exerts its cytotoxicity on HepG2 cells via apoptosis and G2-M arrest. In addition, caspases family activation, regulation of protein expression of bcl-2 family and down regulation of cdc 2 and cyclin B were involved in apoptosis and G2-M arrest induced by it.
出处
《中国中药杂志》
CAS
CSCD
北大核心
2006年第21期1818-1821,共4页
China Journal of Chinese Materia Medica
