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生脉饮加减治疗急性淋巴细胞白血病的分子生物学研究述评。

Review of molecular biological studies on acute lymphoblastic leukemia treated by modified shengmaiyin.

机构信息

Heilongjiang University of Traditional Chinese Medicine, Harbin, China.

The First Affiliated Hospital of Heilongjiang University of Traditional Chinese Medicine, Harbin, China.

出版信息

Medicine (Baltimore). 2023 Jun 9;102(23):e34013. doi: 10.1097/MD.0000000000034013.

DOI:10.1097/MD.0000000000034013
PMID:37335634
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10256333/
Abstract

The objective was to explore the pharmacological mechanism of modified shengmaiyin (MSMY) in the treatment of acute lymphoblastic leukemia (ALL) by network pharmacology analysis. The effective components and predicted targets of MSMY were collected from TCMSP and Swiss target prediction databases, and the related targets of ALL were screened by GeneCards and DisGeNET. The core targets and related signaling pathways of MSMY active ingredients for the treatment of ALL were predicted by protein-protein interaction network (PPI), gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analysis. We identified 172 potential targets for the active components of MSMY, 538 disease targets associated with ALL, and 59 common gene targets. PPI network showed that 27 targets such as triptolide, RAC-alpha serine/threonine-protein kinase (AKT1), vascular endothelial growth factor A and Caspase-3 (CASP3) were the core targets. KEGG enrichment analysis related signaling pathways included cancer pathway, phosphatidylinositol 3 kinase, PI-3K/protein kinase B (PI3K-Akt) signaling pathway, apoptosis and mitogen-activated protein kinase (MAPK) signaling pathway and IL-17 signaling pathway. The effective active components and potential therapeutic targets of MSMY in the treatment of ALL were initially identified by comprehensive network pharmacology, which provides a theoretical basis for further study of the material basis and molecular mechanism of MSMY in the treatment of ALL.

摘要

目的

采用网络药理学分析方法探讨生脉饮加减治疗急性淋巴细胞白血病(ALL)的作用机制。方法:从 TCMSP 和 Swiss target prediction 数据库中收集生脉饮加减的有效成分和预测靶点,通过 GeneCards 和 DisGeNET 筛选与 ALL 相关的靶点,采用蛋白质-蛋白质相互作用网络(PPI)、基因本体(GO)和京都基因与基因组百科全书(KEGG)功能富集分析预测生脉饮加减活性成分治疗 ALL 的核心靶点及相关信号通路。结果:共鉴定出生脉饮加减的 172 个潜在活性成分靶点、538 个与 ALL 相关的疾病靶点和 59 个共有基因靶点。PPI 网络显示,27 个核心靶点如雷公藤内酯醇、RAC-alpha 丝氨酸/苏氨酸蛋白激酶(AKT1)、血管内皮生长因子 A 和 Caspase-3(CASP3)等。KEGG 通路富集分析显示,相关信号通路包括癌症通路、磷脂酰肌醇 3 激酶(PI3K)、PI3K-Akt 信号通路、细胞凋亡和丝裂原活化蛋白激酶(MAPK)信号通路及 IL-17 信号通路。结论:采用综合网络药理学方法初步鉴定了生脉饮加减治疗 ALL 的有效活性成分和潜在治疗靶点,为进一步研究生脉饮加减治疗 ALL 的物质基础和分子机制提供了理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d28d/10256333/5370d917444c/medi-102-e34013-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d28d/10256333/5370d917444c/medi-102-e34013-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d28d/10256333/e422c8bf5b7b/medi-102-e34013-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d28d/10256333/9e4c750f4c63/medi-102-e34013-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d28d/10256333/b86bcb607e9b/medi-102-e34013-g003.jpg
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