紫草素诱导子宫内膜癌Ishikawa细胞凋亡及其机制的研究

Mechanisms of Shikonin - induced Apoptosis in Ishikawa Cells

目的:研究紫草素诱导体外培养的子宫内膜癌Ishikawa细胞凋亡作用及其机制。方法:流式细胞术分析细胞周期分布及凋亡率变化;免疫组化法(SABC法)检测Bcl-2、Bax蛋白的表达。结果:紫草素可诱导细胞凋亡,改变细胞周期分布,多数细胞周期阻滞于G1期,细胞凋亡率差异有统计学意义(P<0.05);紫草素可上调Bax和下调Bcl-2基因蛋白的表达,与空白组对照差异有统计学意义(P<0.05)。结论:紫草素能够诱导子宫内膜癌Ishikawa细胞凋亡,其凋亡机制可能与促进Ishikawa细胞中Bax上调,Bcl-2下调相关。

Objective ： To investigate apoptosis effects and mechanisms of Shikonin on human endometrial carcinoma cell line - Ishikawa. Methods ： Evaluation of cell cycle and apoptosis was ascertained respectively, which used trypan blue exclusion and flow cytometry. The protein expression of Bcl-2 and Bax was detected by immunohistochemical methods. Results-Shikonin could induce the apoptosis of Ishikawa cells, change cell cycle percentage and block cell cycle in G1. There was significant difference in the ap- optotic percent of cell （P 〈 0.05 ） ; Shikonin can up-regulate gene expression of Bax and down - regulate gene expression of Bcl-2. There was significant difference between Shikonin groups and control group（ P 〈 0. 05 ）. Conclusion：Shikonin could promote apop-tosis in Ishikawa cells. The mechanism may be associated with the gene expression of up - regulation of Bax and inhibition of Bcl-2.