Pharmacological evaluation and mechanistic study of compound Xishu Granule in hepatocellular carcinoma

Journal of Traditional Chinese Medical Sciences

Baosheng Zhao¹  Ziying Xu¹  Tieshan Wang¹  Ting Wang¹  Jingxuan Zhang¹  Wenhui Xu¹  Yu Qin¹  Yucong Bi²  Pin Li²  Yuanyuan Shi²  Zhaojuan Guo³ 

[1] Beijing Research Institute of Chinese Medicine, Beijing University of Chinese Medicine, Beijing, 100029, China;School of Life Science, Beijing University of Chinese Medicine, Beijing, 102488, China;School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, 102488, China;

关键词: Compound Xishu Granule;    Hepatocellular carcinoma;    Cell cycle;    CDK1;    Cyclin B1;    PLK1;   

DOI  :  

来源: DOAJ

【 摘 要 】

Objective: In this study, we used HepG2 human hepatocellular carcinoma cells to study the effects of Compound Xishu Granule (CXG) on cell proliferation, apoptosis, and the cell cycle in vitro. We also used a xenograft tumor model to study the anti-tumor effects of CXG and related mechanisms in vivo. Methods: The effect of CXG on cell viability was measured using Cell Counting Kit-8 and a colony formation assay. The effect of CXG on apoptosis and the cell cycle was analyzed using flow cytometry. The in vivo anti-tumor effect of CXG was assessed by measuring the volume change in xenograft tumors after drug administration. The CXG anti-tumor mechanism was studied using western blotting assay to detect cell cycle and apoptotic associated proteins. Results: CXG suppressed HepG2 cell proliferation in a time- and dose-dependent manner in vitro. Colony formation experiments showed that CXG administration for 24 h significantly reduced HepG2 cell formations (P < .01). Flow cytometric analysis showed that CXG treatment for 48 h promoted apoptosis and blocked HepG2 cells in the G2/M phase. Western blotting results showed that Bax was significantly up-regulated and Bcl-2 was down-regulated in graft tumor tissues and HepG2 cells after CXG administration, which increased the Bax/Bcl-2 ratio. PLK1, CDC25C, CDK1, and Cyclin B1 expression were up-regulated. CXG had a good inhibitory effect on graft tumor growth in vivo. Conclusion: CXG has good anti-tumor effects in vitro and in vivo. In vitro, CXG promoted HepG2 cell apoptosis and induced G2/M phase arrest. In vivo, CXG significantly inhibited graft tumor growth. The CXG mechanism in treating hepatocellular carcinoma may be that CXG can induce abnormal apoptotic and cell cycle associated protein expression, leading to mitotic catastrophe and apoptosis.

【 授权许可】

Unknown