| 王硕,程权,廖文宇,等.基于网络药理学探讨香草扶正合剂治疗非小细胞肺癌机制[J].浙江中医药大学学报,2024,48(12):1500-1511. |
| 基于网络药理学探讨香草扶正合剂治疗非小细胞肺癌机制 |
| Investigation of the Mechanism of Xiangcao Fuzheng Mixture in Treating Non-small Cell Lung Cancer Based on Network Pharmacology |
| DOI：10.16466/j.issn1005-5509.2024.12.004 |
| 中文关键词: 细梗香草 香草扶正合剂 非小细胞肺癌 网络药理学 信号通路 动物实验 IL-6 |
| 英文关键词: Lysimachia capillipes Hemsl Xiangcao Fuzheng Mixture non-small cell lung cancer network pharmacology signaling pathway animal experiments IL-6 |
| 基金项目:杭州市卫生科技计划(重点)项目(2018Z02)；国家中医药管理局第七批全国老中医药专家学术经验继承工作室建设项目(国中医药人教函〔2022〕76号)；浙江省名老中医专家传承工作室建设项目(GZS2020029) |
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| 中文摘要: |
| [目的] 基于网络药理学探讨香草扶正合剂(Xiangcao Fuzheng Mixture，XCFZ)治疗非小细胞肺癌的机制。[方法] 使用超高效液相色谱-串联质谱法测定XCFZ的化学成分，通过网络数据库对这些化学成分进行药代动力学筛选、靶点预测、京都基因和基因组百科全书富集分析和蛋白互作(protein-protein interaction，PPI)分析，通过动物实验验证XCFZ的抑瘤效果，测定小鼠肿瘤组织主要核心靶点蛋白表达。[结果] XCFZ含有67种主要成分，药代动力学筛选得到34种化学成分，预测得到486个靶点，涉及176条通路，主要为磷脂酰肌醇-3-激酶-蛋白激酶B(phosphoinositide-3-kinase-protein kinase B，PI3K-AKT)、Ras和辅助性T细胞17(T helper cell 17，Th17)等。PPI分析获得26个核心靶点，度值排在前5位的是RAC-α丝氨酸/苏氨酸蛋白激酶(RAC-alpha serine/threonine-protein kinase，AKT1)、白细胞介素-6(interleukin-6，IL-6)、细胞肿瘤抗原p53(cellular tumor antigen p53，TP53)、丝裂原活化蛋白激酶3(mitogen-activated protein kinase 3，MAPK3)和血管内皮生长因子A(vascular endothelial growth factor A，VEGFA)。动物实验结果显示，与模型组比较，各给药组小鼠肿瘤质量减低(P<0.01)，XCFZ组Bcl-2/Bax比值及AKT1、MAPK3、VEGFA、IL-6蛋白表达水平降低(P<0.01，P<0.05)，TP53蛋白表达水平升高(P<0.05，P<0.01)。[结论] XCFZ对非小细胞肺癌的抑制作用可能与抑制IL-6表达，调节PI3K-AKT、Ras、Th17分化信号通路，抑制VEGFA、MAPK3蛋白表达有关，PI3K-AKT信号通路可能是其发挥抗癌作用的主要通路。 |
| 英文摘要: |
| [Objectives] To investigate the mechanism of Xiangcao Fuzheng Mixture(XCFZ) in treating non-small cell lung cancer based on network pharmacology. [Methods] The chemical constituents of XCFZ were determined by ultraperformance liquid chromatography-tandem mass spectrometry. Pharmacokinetic screening， target prediction， Kyoto Encyclopedia of Gene and Genome enrichment analysis and protein-protein interaction(PPI) analysis were carried out on these chemical components through the online database. Animal experiments verified the anti-tumor effect of XCFZ， and determined the expression of main core target protein in mouse tumor tissue. [Results] XCFZ contains 67 main components， and 34 chemical components are screened out， and 486 targets are predicted， involving 176 pathways， mainly phosphoinositide-3-kinase-protein kinase B(PI3K-AKT)， Ras and T helper cell 17(Th17) cell differentiation. Twenty-six core targets and the top five degrees RAC-alpha serine/threonine-protein kinase(AKT1)， interleukin-6(IL-6)， cellular tumor antigen p53(TP53)， mitogen-activated protein kinase 3(MAPK3) and vascular endothelial growth factor A(VEGFA) were obtained by PPI analysis. The results of animal experiments showed that compared with model group， the tumor quality of mice in each administration group decreased (P<0.01)， the ratio of Bcl-2/Bax and the expression levels of AKT1， MAPK3， VEGFA and IL-6 in XCFZ group decreased (P<0.01， P<0.05)， while the expression level of TP53 protein increased (P<0.05，P<0.01). [Conclusion] The inhibitory effect of XCFZ on the growth of non-small cell lung cancer cells might be related to the inhibition of IL-6 expression to regulate the PI3K-AKT signaling pathway， Ras signaling pathway， Th17 differentiation signaling pathway， inhibition of VEGFA and MAPK3 protein expression， and PI3K-AKT signaling pathway may be the main pathway of its anticancer effect. |
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