冬凌草甲素抑制人胃腺癌细胞生长和诱导凋亡作用研究

Proliferation Inhibition and Apoptosis of Human Gastric Cancer Cells Induced by Oridnin

目的:研究冬凌草甲素对人胃腺癌BGC-823细胞的生长抑制和诱导凋亡的作用及其机制。方法:采用MTT、透射电镜、流式细胞仪等方法对经冬凌草甲素体外作用的BGC-823细胞进行观察和检测。结果:16、32、64μg·mL-1冬凌草甲素能显著抑制BGC-823细胞的生长,并呈浓度-时间依赖性。64μg·mL-1的冬凌草甲素作用24、48、72h的抑制率分别为68·5%、90·8%、94·7%。32μg·mL-1冬凌草甲素作用2h后,电镜下BGC-823细胞的线粒体和内质网增殖肿胀;作用8h后,线粒体和内质网空泡化,内部结构消失,细胞核染色质边集呈凋亡的典型改变;作用24h后,流式细胞仪检测BGC-823细胞G2/M期阻滞,凋亡率为37·8%。结论:冬凌草甲素对人胃腺癌BGC-823细胞具有生长抑制和诱导凋亡作用,生长抑制可能与G2/M细胞周期阻滞有关,诱导凋亡可能通过线粒体和(或)内质网途径起作用。

OBJECTIVE： To investigate the growth inhibition and apoptosis of BGC - 823 gastric cancer cells induced by Oridonin and its mechanism. METHODS： The Oridonin- treated BGC- 823 cells were detected using MTT, transmission electron microscopy （TEM）, TUNEL and flow cytometry （FCM） etc. RESULTS： Oridonin（16, 32, and 64 tlg · mL^-1） significantly inhibited the proliferation of BGC- 823 cells in dose and time dependent manner, with the inhibition rates at 68.5%, 90.8%, and 94.7%, respectively within 24, 48, and 72 h after treatment with 64 μg · mL^-1 Oridnin. When treated with 32 μg · mL^-1 Oridonin for 2 h, mitochondria and endoplasmic reticulum were proliferated and swelled under TEM; At 8 h, vacuolization of mitochondria and endoplasmic reticulum were noted, the internal structure disappeared, and the nuclear chromatin margination vacuolization were in typical apoptosis change; At 24 h, BGC-823 cells were arrested at G2/ M phase, and the apoptosis rate was 37.8% under FCM. CONCLUSION： Oridonin inhibiting proliferation and apoptosis of BGC- 823 cells maybe related to G2/M phase arresting, and Oridonin induce apoptosis of BGC- 823 cells may through mitochondria or endoplasmic reticulum apoptosis pathway.