摘要
目的研究水飞蓟宾-磷脂酰胆碱复合物(Silybin-phosphatidylcholine Compound,SPC)诱导肝癌HepG2细胞凋亡作用及其机制。方法不同浓度SPC处理肝癌HepG2细胞,通过MTT法、细胞形态学观察、流式细胞仪和激光共聚焦显微镜观察SPC对HepG2细胞的生长抑制作用及其细胞凋亡的影响。结果SPC可抑制HepG2细胞的增殖。其GI50为46.8μg/ml;50μg/ml的SPC作用HepG2细胞24h后,细胞出现早期调亡的形态;75μg/ml、100μg/ml的SPC对HepG2细胞凋亡率分别为(17.22±3.45)%和(25.50±5.72)%;50μg/ml、75μg/ml、100μg/ml的SPC作用于HepG2细胞24h后,细胞内的Ca2+浓度显著升高(P<0.05,P<0.01)。结论SPC能够诱导肝癌细胞系HepG2细胞凋亡,其机制与SPC升高细胞内Ca2+浓度有关。
Objective To investigate the apoptosis effect of Silybin - phosphatidylcholine Compound (SPC) on human hepatoma cell HepG2 and its mechanisms. Methods HepG2 cells were treated with differetent concentrations of SPC. MTT assay was used to observe the inhibitory rate of SPC, and fluoreacence microscope, flow cytometry and laser conlocal microscopy were used to observe the influence of SPC on cell apoptosis of HepG2. Results The proliferation of HepG2 was inhibited by different concentration of SPC and the GI50 is 46.8μg/ml;Afler treating with 50 μg/ml of SPC for 24 h, morphological changes of early apoptosis were observed. At the dosage of 75 μg/ml and 100 μg/ml, SPC could promote the apoptosis of HepG2 cell and the apoptotic rates are ( 17.22±3.45)% and (25.50±5.72)% respeatively. After treating with 50 μg/ml, 75 μg/ml, 100 μg/m of SPC for 24 h, the intracellular Ca^2+ : level was remarkably increased ( P 〈 0.05, P 〈 0.01 ). Conclusions SPC can induce cell apoptosis of HepG2 and the mechanism is related with the increase of intracellular Ca^2+.
出处
《医学信息(内.外科版)》
2009年第2期147-149,共3页
Medical Information Operations Sciences Fascicule