紫草素体外对人结肠癌生长抑制的作用

Inhibitory Effect of Shikonin on the Growth of Human Colon Cancer Cells in Vitro

目的研究紫草素对体外培养的人结肠癌细胞HCT116增殖的影响,并初步探讨其潜在的调节作用机制。方法体外正常培养的HCT116细胞分别给予不同浓度的紫草素刺激,MTT法检测HCT116细胞的增殖情况,AnnexinV-FITC/PI双染后,流式检测HCT116细胞凋亡,qRT-PCR检测细胞中Bcl-2、Bax的mRNA表达,Westernblot检测HCT116细胞中Akt蛋白磷酸化水平。结果10~80μg/mL浓度的紫草素对HCT116细胞增殖均有明显的抑制作用,并能促进凋亡;随紫草素浓度增加,HCT116细胞Bcl-2的mRNA表达逐渐下降(P<0.05),Bax的mRNA表达水平逐渐升高(P<0.05),p-Akt蛋白表达逐渐减少(P<0.05)。结论紫草素可以诱导体外培养的人结肠癌细胞HCT116发生凋亡,其机制可能与抑制PI3K/Akt信号通路的激活,进一步降低Bcl-2mRNA表达,增加Bax的mRNA表达有关。

Objective To investigate the effects and the mechanismof Shikonin on the proliferation of human colon cancer HCT116 cells.Methods HCT116 cells were treated with different concentrations of shikonin,MTT assay was used to detect the proliferation of HCT116 cell,Annexin V-FITC/PI double staining and flow cytometry were used to detect the apoptosis rate,Bcl-2 and Bax mRNA expression were analyzed by qRT-PCR,phosphorylated Akt expression was detected by western-blot.Results 10-80 μg/mL of shikonin significantly inhibited proliferation and promote apoptosis on HCT116.The expression of Bcl-2 mRNA was decreased and the expression of Bax mRNA were increased by Shikonin(P < 0.05);The expression of p-Akt protein was decreased by Shikonin(P < 0.05).Conclusion Shikonin can promote the apoptosis of colon cancer HCT116 cells, the mechanism may be related to inhibiting PI3K/Akt signaling pathway,decreasing Bcl-2 mRNA expression and increasing Bax mRNA expression.