首页|基于网络药理学和分子对接技术的2,3-吲哚醌抗少弱精症机制研究

基于网络药理学和分子对接技术的2,3-吲哚醌抗少弱精症机制研究

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为研究 2,3-吲哚醌(isatin,ISA)治疗少弱精症的可能作用靶点和作用机制,基于公共数据库分别获取ISA作用靶点和少弱精症相关疾病靶点,确定交集靶点,采用Cytoscape 软件获取核心靶点.通过GO 功能富集和KEGG通路分析交集靶点,采用分子对接预测 ISA与靶点蛋白的结合能力.研究结果显示,ISA干预少弱精症主要涉及氧化应激、细胞凋亡和炎症等生物学过程,并与 p53 信号通路、细胞衰老通路和 IL-17 信号通路密切相关;经筛选确定 8 个核心靶点,ISA与其中 6 个核心靶点稳定结合.这表明,ISA可能通过作用于核心靶点CASP3、TP53、ESR1、PTGS2、TNF和ANXA5,调控 p53 信号通路和 IL-17 信号通路发挥抗少弱精症作用.
Mechanistic Study of Isatin Against Oligoasthenozoospermia Based on Network Pharmacology and Molecular Docking
To investigate the potential targets and mechanisms of isatin(ISA)in the treatment of oligoas-thenozoospermia,targets of ISA and disease-related targets were identified utilizing public databases to find intersecting targets.Core targets were then determined using Cytoscape software.GO functional en-richment and KEGG pathway analyses on the intersecting targets were conducted,and molecular docking was used to predict the binding affinity of ISA with core target proteins.The results indicate that ISA's in-tervention in oligoasthenozoospermia primarily involves biological processes such as oxidative stress,apop-tosis,and inflammation,and is closely related to the p53 signaling pathway,the cell senescence pathway,and the IL-17 signaling pathway.After screening,eight core targets were identified,with ISA stably bind-ing to six of them.Those suggest that ISA may exert its anti-oligoasthenospermia effects by modulating the p53 signaling pathway and the IL-17 signaling pathway through core targets including CASP3,TP53,ESR1,PTGS2,TNF and ANXA5.

isatinnetwork pharmacologyoligoasthenozoospermiamolecular docking

倪倍倍、代梦、毕晓林、赵志臣、岳旺、隋忠国

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青岛大学附属医院药学部,青岛 266000

青岛大学附属医院营养科,青岛 266000

青岛黄海学院护理与健康学院,青岛 266427

2,3-吲哚醌 网络药理学 少弱精症 分子对接

国家自然科学基金

30070867

2024

青岛大学学报(自然科学版)
青岛大学

青岛大学学报(自然科学版)

影响因子:0.248
ISSN:1006-1037
年,卷(期):2024.37(2)
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