BRIEF RESEARCH REPORT article
Front. Cell. Infect. Microbiol.
Sec. Veterinary and Zoonotic Infection
Volume 15 - 2025 | doi: 10.3389/fcimb.2025.1623860
This article is part of the Research TopicUnveiling Host-Pathogen Interactions: Insights into Animal Cellular Immunity and Novel Diagnostics - Volume IIView all 14 articles
Assessing the Potential Impact of Salidroside on Chikungunya Virus-Induced Acute Interstitial Nephritis via Network Pharmacology, Molecular Docking and In Vitro Experiments
Provisionally accepted
Sheng Cheng1
Jialiang Xin1,2,3
Tianran Zhang4
Yuling Zhang2,3Chengxi Ji2Lulu Kang2
Xiangyu ZHU2*
He Zhang3*
Wei Wang2,3
Xinfei Liao5*- 1Key Laboratory of Animal Disease and Human Health of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University,, Chengdu, China
- 2Wenzhou University, Wenzhou, China
- 3Changchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, China
- 4Wenzhou Municipal Center for Disease Control and Prevention, Wenzhou Municipal Institute of Health Supervision, Wenzhou, China
- 5Wenzhou Vocational and Technical College, Wenzhou, China
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Chikungunya virus (CHIKV) infection is often linked to acute interstitial nephritis (AIN) in fatal cases. Given the global spread of CHIKV and the lack of targeted antiviral treatments, there is an urgent need for effective therapeutic strategies against CHIKV-induced AIN. This study explored the therapeutic potential of salidroside (Sal) using an integrative approach involving network pharmacology, molecular docking and in vitro validation. Network pharmacology analysis identified 18 overlapping targets between Sal and AIN, including TNF, IL6 and AKT1. Molecular docking revealed strong binding affinities between Sal and key pathway proteins (Vina scores < -6), notably TNF, IL6 and BCL2. In vitro assays using CHIKV-infected 293T cells demonstrated that Sal (7.8125-2000 μM) enhanced cell viability by 8.9-25.9%, with the greatest effect observed at 1000 μM, without significantly altering viral replication.Mechanism analysis using the KEGG and FerrDB databases implicated apoptosis and ferroptosis in CHIKV-induced AIN pathogenesis. RT-qPCR analysis confirmed that Sal significantly downregulated ferroptosis-related genes (IL-6, IL-1β, SIRT1, PARP1, HMOX1) and apoptosis-associated markers (Bax, TNF-α, PARP1) in infected cells.Consistent with these findings, molecular docking demonstrated that Sal binds strongly to the ferroptosis-related protein GPX4 (Vina score: -6.3) and the apoptosis regulator NFKB1 (Vina score: -6.0). These results suggest that Sal is a promising therapeutic candidate for the treatment of CHIKV-induced AIN.
Keywords: CHIKV, Salidroside, Network Pharmacology, molecular docking, ferroptosis, Apoptosis
Received: 06 May 2025; Accepted: 30 Jun 2025.
Copyright: © 2025 Cheng, Xin, Zhang, Zhang, Ji, Kang, ZHU, Zhang, Wang and Liao. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Xiangyu ZHU, Wenzhou University, Wenzhou, China
He Zhang, Changchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, China
Xinfei Liao, Wenzhou Vocational and Technical College, Wenzhou, China
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