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Abstract：
UNASSIGNED: To explore the mechanism of PG against acute lymphoblastic leukaemia (ALL) by network pharmacology and experimental verification in vitro.
UNASSIGNED: First, the biological activity of PG against B-ALL was determined by CCK-8 and flow cytometry. Then, the potential targets of PG were obtained from the PharmMapper database. ALL-related genes were collected from the GeneCards, OMIM and PharmGkb databases. The two datasets were intersected to obtain the target genes of PG in ALL. Then, protein interaction networks were constructed using the STRING database. The key targets were obtained by topological analysis of the network with Cytoscape 3.8.0 software. In addition, the mechanism of PG in ALL was confirmed by protein‒protein interaction, gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses. Furthermore, molecular docking was carried out by AutoDock Vina. Finally, Western blotting was performed to confirm the effect of PG on NALM6 cells.
UNASSIGNED: PG inhibited the proliferation of NALM6 cells. A total of 174 antileukaemic targets of PG were obtained by network pharmacology. The key targets included AKT1, MAPK14, EGFR, ESR1, LCK, PTPN11, RHOA, IGF1, MDM2, HSP90AA1, HRAS, SRC and JAK2. Enrichment analysis found that PG had antileukaemic effects by regulating key targets such as MAPK signalling, and PG had good binding activity with MAPK14 protein (-8.9 kcal/mol). PG could upregulate the expression of the target protein p-P38, induce cell cycle arrest, and promote the apoptosis of leukaemia cells.
UNASSIGNED: MAPK14 was confirmed to be one of the key targets and pathways of PG by network pharmacology and molecular experiments.
UNASSIGNED: First, the biological activity of PG against B-ALL was determined by CCK-8 and flow cytometry. Then, the potential targets of PG were obtained from the PharmMapper database. ALL-related genes were collected from the GeneCards, OMIM and PharmGkb databases. The two datasets were intersected to obtain the target genes of PG in ALL. Then, protein interaction networks were constructed using the STRING database. The key targets were obtained by topological analysis of the network with Cytoscape 3.8.0 software. In addition, the mechanism of PG in ALL was confirmed by protein‒protein interaction, gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses. Furthermore, molecular docking was carried out by AutoDock Vina. Finally, Western blotting was performed to confirm the effect of PG on NALM6 cells.
UNASSIGNED: PG inhibited the proliferation of NALM6 cells. A total of 174 antileukaemic targets of PG were obtained by network pharmacology. The key targets included AKT1, MAPK14, EGFR, ESR1, LCK, PTPN11, RHOA, IGF1, MDM2, HSP90AA1, HRAS, SRC and JAK2. Enrichment analysis found that PG had antileukaemic effects by regulating key targets such as MAPK signalling, and PG had good binding activity with MAPK14 protein (-8.9 kcal/mol). PG could upregulate the expression of the target protein p-P38, induce cell cycle arrest, and promote the apoptosis of leukaemia cells.
UNASSIGNED: MAPK14 was confirmed to be one of the key targets and pathways of PG by network pharmacology and molecular experiments.
摘要：
UNASSIGNED：通过网络药理学和体外实验验证，探讨PG抗急性淋巴细胞白血病（ALL）的机制。
未经批准：首先，通过CCK-8和流式细胞术测定PG抗B-ALL的生物学活性。然后，PG的潜在靶标来自PharmMapper数据库.ALL相关基因是从GeneCards收集的，OMIM和PharmGkb数据库。将两个数据集相交以获得ALL中PG的靶基因。然后，使用STRING数据库构建蛋白质相互作用网络。利用Cytoscape3.8.0软件对网络进行拓扑分析,得到关键目标。此外,PG在ALL中的机制得到了蛋白质-蛋白质相互作用的证实，基因本体论和京都百科全书的基因和基因组途径富集分析。此外，分子对接由AutoDockVina进行。最后,进行Western印迹以证实PG对NALM6细胞的作用。
未授权：PG抑制NALM6细胞增殖。通过网络药理学总共获得了174个PG的抗白血病靶标。关键靶点包括AKT1、MAPK14、EGFR、ESR1,LCK,PTPN11RHOA,IGF1,MDM2,HSP90AA1,HRAS,SRC和JAK2。富集分析发现，PG通过调节关键靶标（如MAPK信号）具有抗白血病作用，PG与MAPK14蛋白具有良好的结合活性（-8.9kcal/mol）。PG可以上调靶蛋白p-P38的表达，诱导细胞周期停滞，促进白血病细胞凋亡。
UNASSIGNED：通过网络药理学和分子实验证实MAPK14是PG的关键靶标和途径之一。
未经批准：首先，通过CCK-8和流式细胞术测定PG抗B-ALL的生物学活性。然后，PG的潜在靶标来自PharmMapper数据库.ALL相关基因是从GeneCards收集的，OMIM和PharmGkb数据库。将两个数据集相交以获得ALL中PG的靶基因。然后，使用STRING数据库构建蛋白质相互作用网络。利用Cytoscape3.8.0软件对网络进行拓扑分析,得到关键目标。此外,PG在ALL中的机制得到了蛋白质-蛋白质相互作用的证实，基因本体论和京都百科全书的基因和基因组途径富集分析。此外，分子对接由AutoDockVina进行。最后,进行Western印迹以证实PG对NALM6细胞的作用。
未授权：PG抑制NALM6细胞增殖。通过网络药理学总共获得了174个PG的抗白血病靶标。关键靶点包括AKT1、MAPK14、EGFR、ESR1,LCK,PTPN11RHOA,IGF1,MDM2,HSP90AA1,HRAS,SRC和JAK2。富集分析发现，PG通过调节关键靶标（如MAPK信号）具有抗白血病作用，PG与MAPK14蛋白具有良好的结合活性（-8.9kcal/mol）。PG可以上调靶蛋白p-P38的表达，诱导细胞周期停滞，促进白血病细胞凋亡。
UNASSIGNED：通过网络药理学和分子实验证实MAPK14是PG的关键靶标和途径之一。
