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桔梗皂苷D可诱导HepG2肝癌细胞凋亡,并抑制其黏附、迁移和侵袭。

Platycodin D induces apoptosis, and inhibits adhesion, migration and invasion in HepG2 hepatocellular carcinoma cells.

作者信息

Li Ting, Xu Wen-Shan, Wu Guo-Sheng, Chen Xiu-Ping, Wang Yi-Tao, Lu Jin-Jian

机构信息

State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China E-mail :

出版信息

Asian Pac J Cancer Prev. 2014;15(4):1745-9. doi: 10.7314/apjcp.2014.15.4.1745.

Abstract

BACKGROUND

Platycodin D (PD), a triterpenoid saponin isolated from the Chinese medicinal herb Platycodonis radix, possesses anti-cancer effects in several cancer cell lines. The aim of this study was to evaluate its anti- cancer activities in hepatocellular carcinoma cells.

MATERIALS AND METHODS

MTT and colony formation assays were performed to evaluate cell proliferation, along with flow cytometry and Western blotting for apoptosis. Cell adhesion was tested by observing cellular morphology under a microscope, while the transwell assay was employed to investigate the cell migration and invasion.

RESULTS

PD concentration-dependently inhibited cell proliferation in both HepG2 and Hep3B cells, and significantly suppressed colony formation and induced apoptosis in HepG2 cells. The protein levels of cleaved poly ADP-ribose polymerase (PARP) and Bax were up-regulated while that of survivin was down-regulated after treatment with PD. Moreover, PD not only obviously suppressed the adhesion of HepG2 cells to Matrigel, but also remarkably depressed their migration and invasion induced by 12-O-tetradecanoylphorbol 13-acetate (TPA).

CONCLUSIONS

PD presents anti-cancer potential in hepatocellular carcinoma cells via inducing apoptosis, and inhibiting cell adhesion, migration and invasion, indicating promising features as a lead compound for anti-cancer agent development.

摘要

背景

桔梗皂苷D(PD)是从中药材桔梗中分离得到的一种三萜皂苷,在多种癌细胞系中具有抗癌作用。本研究旨在评估其在肝癌细胞中的抗癌活性。

材料与方法

采用MTT法和集落形成试验评估细胞增殖,通过流式细胞术和蛋白质免疫印迹法检测细胞凋亡。通过显微镜观察细胞形态检测细胞黏附,采用Transwell试验研究细胞迁移和侵袭。

结果

PD浓度依赖性地抑制HepG2和Hep3B细胞的增殖,并显著抑制HepG2细胞的集落形成并诱导其凋亡。PD处理后,裂解的聚ADP核糖聚合酶(PARP)和Bax的蛋白水平上调,而生存素的蛋白水平下调。此外,PD不仅明显抑制HepG2细胞与基质胶的黏附,还显著抑制12-O-十四酰佛波醇-13-乙酸酯(TPA)诱导的细胞迁移和侵袭。

结论

PD通过诱导凋亡以及抑制细胞黏附、迁移和侵袭,在肝癌细胞中呈现抗癌潜力,表明其作为抗癌药物开发的先导化合物具有良好特性。

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