Gao Wei, Xu Hua Liang Yanlei Li Yuanyuan Liu Yanxia
The Department of Modern and Traditional Medicine, The Tumor Hospital of Qingdao, Qingdao, 266000, China.
J BUON. 2019 Mar-Apr;24(2):549-554.
In this study we examined the anticancer effects of methanolic root extract of Prunella Vulgaris (PVE) against the MCF-5 breast cancer (BC) cell line along with its mode of action.
The proliferation rate of the MCF-5 cells was assessed by MTT assay. Apoptosis was confirmed by acridine orange (AO)/ethidium bromide (EB) and annexin V/propidium iodide (PI) staining. DNA damage was checked by comet assay. Cell cycle analysis was performed by flow cytometry. Protein expression was determined by western blotting. In vivo evaluation of the extract was carried out in xenografted tumor mice models.
PVE inhibited the growth of the MCF-5 cells and exhibited an IC50 value of 25 µg/ml. The investigation of underlying mechanism revealed that PVE triggered apoptotic cell death of the MCF-5 cells which was also associated with enhancement of the expression of Bax and decrease in the expression of Bcl-2. PVE also caused arrest of the cells in the G2/M phase of the cell cycle and also exerted the anti-angiogenic effects. In vivo evaluation of PVE showed that it could inhibit the tumor weight and volume, suggestive of the anticancer potential of PVE.
The root extract of Prunella vulgaris in this study was shown to exert potent anticancer effects in MCF-7 human BC cells both in vitro and in vivo, accompanied with apoptosis induction, inhibition of angiogenesis, cell cycle arrest, and modulation of PI3K/AKT signaling pathway.
在本研究中,我们研究了夏枯草甲醇根提取物(PVE)对MCF - 5乳腺癌(BC)细胞系的抗癌作用及其作用方式。
通过MTT法评估MCF - 5细胞的增殖率。通过吖啶橙(AO)/溴化乙锭(EB)和膜联蛋白V/碘化丙啶(PI)染色确认细胞凋亡。通过彗星试验检查DNA损伤。通过流式细胞术进行细胞周期分析。通过蛋白质印迹法测定蛋白质表达。在异种移植肿瘤小鼠模型中对提取物进行体内评估。
PVE抑制MCF - 5细胞的生长,IC50值为25μg/ml。对潜在机制的研究表明,PVE引发MCF - 5细胞的凋亡性细胞死亡,这也与Bax表达的增强和Bcl - 2表达的降低有关。PVE还导致细胞在细胞周期的G2/M期停滞,并发挥抗血管生成作用。PVE的体内评估表明它可以抑制肿瘤重量和体积,提示PVE的抗癌潜力。
本研究中的夏枯草根提取物在体外和体内均显示出对MCF - 7人乳腺癌细胞具有强大的抗癌作用,伴有诱导凋亡、抑制血管生成、细胞周期停滞以及调节PI3K/AKT信号通路。