Mechanism of nitidine chloride against Talaromyces marneffei,determined through network pharmacology
10.3969/j.issn.1002-2694.2025.00.049
- VernacularTitle:基于网络药理学探讨氯化两面针碱抗马尔尼菲篮状菌的作用机制
- Author:
Meng ZHANG
1
;
Wudi WEI
;
Baili ZHAN
;
Xiaotao HE
;
Xiaoting XIE
;
Junjun JIANG
;
Li YE
;
Hao LIANG
Author Information
1. 广西医科大学生命科学研究院,中国(广西)-东盟新发传染病联合实验室,南宁 530021
- Publication Type:Journal Article
- Keywords:
nitidine chloride;
Talaromyces marneffei;
network pharmacology;
MAPK signaling pathway
- From:
Chinese Journal of Zoonoses
2025;41(7):675-681
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed at exploring the mechanism underlying the effects of nitidine chloride against Talaromyces marnef-fei through network pharmacology analysis.We collected NC and TM action targets from various databases;constructed a protein-protein interaction(PPI)network by using common drug and disease targets;and performed KEGG pathway and GO enrichment analy-ses.In vitro cellular experiments were conducted to test the antibacterial ability of NC at various concentrations,qPCR was used to de-tect the mRNA expression of genes in the target pathway,and WB was used to examine the expression of proteins associated with tar-get signaling pathways in cells.We identified 153 target genes for NC and 2 095 target genes for TM,among which 23 targets over-lapped.By integrating the PPI network with KEGG enrichment analysis,we selected key target genes in the MAPK signaling pathway,such as FLT1,FLT3,CD38,and PRF1.The CFU results indicated that NC had favorable antibacterial capability.Moreover,qPCR demonstrated that NC downregulated the mRNA expression of FLT1,FLT3,and RPS6KA3,and upregulated the mRNA expression of MAP3K8.WB findings indicated that NC downregulated the expression of RSK2,VEGF,and FLT3 proteins,and upregulated the ex-pression of MAP3K8 protein.NC may exert its anti-TM effects by downregulating the expression of RSK2,VEGF,and FLT3 proteins,thereby inhibiting MAPK pathway activation.The potential targets and signaling pathways underlying NC's anti-TM action may pro-vide new insights to guide the clinical application of NC.
