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作 者:白凤 齐君 张燕[1] 董志强 BAI Feng;QI Jun;ZHANG Yan(Clinical Pharmacy,First Affiliated Hospital of Baotou Medical College,Inner Mongolia University of Science and Technology,Baotou 014010,China)
机构地区:[1]内蒙古科技大学包头医学院第一附属医院,内蒙古包头014010
出 处:《中国处方药》2024年第10期25-28,共4页Journal of China Prescription Drug
基 金:包头医学院科学研究基金项目(BYJJ-QWB202226)。
摘 要:目的采用网络药理学探索氧化苦参碱(OM)治疗甲状腺癌(TC)的作用机制。方法通过TCMSP等数据库筛选OM用于治疗TC的相关作用靶点;通过GEO基因表达数据库、TTD靶点数据库、Drugbank、GeneCards数据库等获得TC相关疾病靶点,通过STRING数据库构建蛋白互作网络(PPI);使用Cytocape3.9.0软件构建网络图;应用DAVID数据库进行基因本体论(GO)和京都基因与基因组百科全书(KEGG)通路分析。结果得到141个OM相关的药物靶点和1405个TC相关的疾病靶点;根据degree值筛选出核心靶点,排名靠前的靶点有:肿瘤蛋白P53(TP53)、蛋白激酶B(AKT1)、促分裂原活化蛋白激酶3(MAPK3)、酪氨酸蛋白激酶(SRC)、促分裂原活化蛋白激酶1(MAPK1)等;GO功能富集显示,OM抗TC的生物学进程主要涵盖细胞分解代谢过程、B淋巴细胞瘤-2蛋白家族复合物、蛋白激酶调节活性等;KEGG信号通路主要涉及磷脂酶酰肌醇3-激酶-蛋白激酶B信号通路(PI3K-Akt signaling pathway)、缺氧诱导因子-1信号通路(HIF-1 signaling pathway)、Janus激酶-信号转导和转录激活因子信号通路(JAK-STAT signaling pathway)等。结论OM治疗TC的机制涉及多个关键靶点和多条信号通路,各靶点与各通路之间产生的交叉作用,可能会抑制炎症反应和加速癌症细胞凋亡从而治疗TC。Objective To explore the action mechanism of oxymatrine(OM)in the treatment of TC using network pharmacology.Methods Screening the relevant targets of OM for the treatment of TC through databases such as TCMSP;Obtain TC related disease targets through GEO gene expression database,TTD target database,Drugbank,GeneCards database,etc.,and construct Protein-Protein Interaction(PPI)through STRING database.Build a network diagram using Cytocape3.9.0 software;Apply DAVID database for GO and KEGG pathway analysis.Results 141 OM related drug targets and 1405 TC related disease targets were obtained;Based on the degree value,core targets were selected,and the top ranked targets include tumor protein P 53(TP53),protein kinase B(AKT1),mitogen activated protein kinase 3(MAPK3),tyrosine protein kinase(SRC),mitogen activated protein kinase 1(MAPK1),etc;GO functional enrichment shows that the biological processes of OM against TC mainly include cellular catabolism,B-lymphomatoma-2 protein family complexes,and protein kinase regulatory activity;The KEGG signaling pathway mainly involves the PI3K-Akt signaling pathway,HIF-1 signaling pathway,and JAK-STAT signaling pathway.Conclusion The mechanism of OM in treating TC involves multiple key targets and signaling pathways,and the cross effects between each target and pathway may inhibit inflammatory response and accelerate cancer cell apoptosis,thereby treat TC.
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