Network Pharmacology-Based Study on the Mechanism of Bushen-Jianpi Decoction in Liver Cancer Treatment

被引:15
|
作者
Wu, Rong [1 ]
Li, Xiao-Yan [1 ]
Wang, Wen-Hai [2 ]
Cai, Fei-Fei [1 ]
Chen, Xiao-Le [1 ]
Yang, Meng-Die [1 ]
Pan, Qiu-Sha [1 ]
Chen, Qi-Long [1 ]
Zhou, Rong-Yao [3 ]
Su, Shi-Bing [1 ]
机构
[1] Shanghai Univ Tradit Chinese Med, Inst Interdisciplinary Integrat Med Res, Res Ctr Tradit Chinese Med Complex Syst, Shanghai, Peoples R China
[2] Shanghai Univ Tradit Chinese Med, Shanghai Baoshan Hosp Integrated Tradit Chinese M, Shanghai 201999, Peoples R China
[3] Shanghai Univ Tradit Chinese Med, Dept Med Oncol, Shuguang Hosp, Shanghai 201203, Peoples R China
基金
美国国家科学基金会;
关键词
DEATH;
D O I
10.1155/2019/3242989
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
To investigate the mechanism of a Bushen-Jianpi decoction (BSJPD) in liver cancer (LC) treatment, we analyzed clinical therapy data, conducted network pharmacology analysis, and performed pharmacological experimental verification in vitro and in vivo. The univariate analysis of clinical therapy showed that the BSJPD was protective factor (p < 0.05). The network pharmacology analysis showed that 9 compounds were important nodes of BSJPD-LC therapy network. In experimental verification, the rate of apoptosis increased in the liver tumors of mice treated with the BSJPD (p < 0.05); drug serum with 20 % BSJPD inhibited cell viability (p < 0.05) and reduced the expression of MK, the Bcl-xL/BAD ratio, and the levels of p53 and p-Akt in HepG2 cells. Moreover, licochalcone A, alisol B, and hederagenin inhibited cell viability (p < 0.05), induced cell apoptosis (p < 0.01), reduced p-Akt levels, and increased cleaved-CASP3 (p < 0.05) and p53 expression levels in HepG2 cells. These data suggest that the BSJPD prolongs the survival of LC patients and induces apoptosis and that it may be associated with the regulation of PI3K, Akt, p53, CASP3, and Bcl-xL/BAD expression.
引用
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页数:13
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