| 引用本文:赖瑞，史晓光，左禧萌，汪唐顺，刘洁丽，杨臻瑞，冯雪，王玉坤，高爽，孙萍.紫草素对乳腺恶性肿瘤细胞凋亡及PI3K/AKT信号通路的影响[J].世界中医药,2023,(06):. |
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| 紫草素对乳腺恶性肿瘤细胞凋亡及PI3K/AKT信号通路的影响 |
| Effects of Alkannin on Apoptosis and PI3K/Akt Signaling Pathway in Breast Cancer Cells |
| 投稿时间：2021-07-17 |
| DOI：10.3969/j.issn.1673-7202.2023.06.009 |
| 中文关键词: 紫草素 乳腺恶性肿瘤 细胞凋亡 高转移恶性乳腺癌细胞系 原位雌激素受体阳性乳腺癌细胞系 磷脂酰肌醇3激酶 |
| English Keywords:Alkannin Breast cancer Apoptosis MDA-MB-231 MCF-7 Phosphoinositide 3-kinase |
| 基金项目:湖北省陈孝平科技发展基金项目（CXPJJH12000002-2020010）——三阴性乳腺癌病人术后应用槐耳颗粒的疗效及机制研究 |
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| 中文摘要: |
| 目的：探讨紫草素对乳腺恶性肿瘤MDA-MB-231和MCF-7细胞凋亡以及PI3K/AKT信号通路表达的影响。方法：将MDA-MB-231及MCF-7细胞系用含不同浓度紫草素的完全培养基(分组为0、0.2、0.4、0.8、1.0 mg/mL)进行培养，CCK-8法检测细胞活性，Annexin V-FTIC/PI染色后流式细胞仪检测细胞凋亡情况，蛋白质印迹法测定细胞内PI3K/AKT表达情况。结果：与空白对照组（0 mg/mL）比较，紫草素浓度为0.8 mg/mL以上时对乳腺癌MDA-MB-231及MCF-7细胞生长具有显著抑制作用，最佳作用浓度为1.0 mg/mL；与空白对照组比较，MDA-MB-231及MCF-7细胞的凋亡水平随紫草素浓度增加而增加，且差异有统计学意义（P<0.05）；与空白对照组比较，经紫草素处理的MDA-MB-231及MCF-7细胞PI3K表达均出现不同程度下降，差异有统计学意义（P<0.05）。结论：紫草素具有针对MDA-MB-231及MCF-7乳腺癌细胞系的抗肿瘤作用，其机制可能与其抑制PI3K/AKT信号通路有关。 |
| English Summary: |
| To investigate the effects of alkannin on the apoptosis and phosphoinositide 3-kinase(PI3K)/protein kinase B(Akt) signaling pathway in malignant breast cell lines MDA-MB-231 and MCF-7.Methods:MDA-MB-231 and MCF-7 cells were cultured in the complete media containing different concentrations of alkannin(0，0.2，0.4，0.8，and 1.0 mg/mL).The cell viability，apoptosis，and PI3K/Akt expression were determined by CCK-8 assay，Annexin V-FTIC/PI staining-flow cytometry，and western blotting，respectively.Results:Compared with the blank control group(0 mg/mL)，alkannin at a concentration of 0.8 mg/mL and higher significantly inhibited the growth of MDA-MB-231 and MCF-7 cells，and that of 1.0 mg/L demonstrated the best performance.The apoptosis of MDA-MB-231 and MCF-7 cells increased with the rise in alkannin concentration(P<0.05).Compared with the blank control group，alkannin down-regulated the expression of PI3K in MDA-MB-231 and MCF-7 cells(P<0.05).Conclusion:Alkannin may exert the anti-tumor effects on MDA-MB-231 and MCF-7 cells by inhibiting the PI3K/Akt signaling pathway. |
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