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

机译:基于网络药理学的补肾健脾汤治疗肝癌的机制研究

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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 PI3K, 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.
机译:为了研究补肾健脾汤(BSJPD)在肝癌(LC)治疗中的作用机理,我们分析了临床治疗数据,进行了网络药理分析,并在体内和体外进行了药理实验验证。临床治疗的单因素分析表明BSJPD是保护因子(p <0.05)。网络药理分析表明,9种化合物是BSJPD-LC治疗网络的重要节点。在实验验证中,用BSJPD处理的小鼠肝肿瘤中的凋亡率增加(p <0.05);含20%BSJPD的药物血清可抑制细胞活力(p <0.05),并降低HepG2细胞中PI3K的表达,Bcl-xL / BAD比以及p53和p-Akt的水平。此外,licochalcone A,alisol B和hederagenin抑制细胞活力(p <0.05),诱导细胞凋亡(p <0.01),降低p-Akt水平,并增加HepG2中CASP3的切割水平(p <0.05)和p53表达水平。细胞。这些数据表明,BSJPD延长了LC患者的生存时间并诱导了细胞凋亡,并且它可能与PI3K,Akt,p53,CASP3和Bcl-xL / BAD表达的调节有关。

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