ORIGINAL RESEARCH article
Front. Vet. Sci.
Sec. Veterinary Infectious Diseases
Volume 12 - 2025 | doi: 10.3389/fvets.2025.1663508
This article is part of the Research TopicHigh-Impact Respiratory RNA Virus Diseases, Volume IIView all 8 articles
Potential mechanisms of zinc sulfate in inhibiting porcine reproductive and respiratory syndrome virus replication: attenuation of oxidative stress, inflammatory response, and apoptosis
Provisionally accepted
- Shanxi Agricultural University, Jinzhong, China
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This study aimed to elucidate the mechanism of zinc sulfate against porcine reproductive and respiratory syndrome virus (PRRSV) through transcriptomic data and experimental validation.Methods: Initially, the expression of PRRSV N gene and protein were quantified using qPCR and immunofluorescence, respectively. High-throughput RNA sequencing was performed to analyze global gene expression changes in PRRSV-infected Marc-145 cells treated with zinc sulfate.Transcriptomic data were subjected to bioinformatic analyses, including Venn diagram assessments, protein-protein interaction network construction using the STRING database, and identification of hub genes via Cytoscape 3.10.0. Functional enrichment analysis of Gene Ontology and KEGG pathways were performed using R (v4.4.3). Subsequently, oxidative stress parameters in PRRSVinfected Marc-145 cells treated with zinc sulfate were detected using biochemical assays. The modulatory effects of zinc sulfate on inflammatory response and apoptosis were evaluated through qPCR and western blot, measuring the expression of cytokines (IL-6, IL-8, TNF-α, IL-10), apoptosis-related proteins (Caspase-3, Bax, Bcl-2), and key components of the NF-κB pathway.Finally, flow cytometry was employed to assess cellular apoptosis rates.The result demonstrated that zinc sulfate significantly suppressed PRRSV replication. The transcriptomic analysis revealed that compared to the PRRSV-infected group, there were 14 upregulated and 50 downregulated targets in zinc sulfate treatment group. Among these, ten core downregulated and upregulated targets were well enriched in the inflammation and apoptosis pathways, respectively. The experimental verification results demonstrated that compared to the PRRSV-infected group, zinc sulfate treatment significantly dimininshed intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) levels, while elevating the enzymatic activities of superoxide dismutase (SOD) and catalase (CAT) (p < 0.05). It also suppressed the expression of IL-6, IL-8, TNF-α, while upregulating IL-10 (p < 0.05). In addition to, it also upregulated the 2 phosphorylation levels of IκBα and p65 (p < 0.05), and decreased the expression of Caspase-3, cleaved-Caspase-3, Bax, while enhancing Bcl-2 (p < 0.05). Simultaneousy, flow cytometry analysis further confirmed that zinc sulfate substantially attenuated late-stage and overall apoptosis rates in PRRSV-infected cells (p < 0.05).These results implied that zinc sulfate restricted oxidative stress, diminished inflammatory response and induced apoptotic suppression to confer protection against PRRSV infection.
Keywords: Zinc Sulfate, Porcine Reproductive and Respiratory Syndrome Virus, Transcriptomic Analysis, Oxidative Stress, Inflammatory factors, Apoptosis
Received: 10 Jul 2025; Accepted: 11 Aug 2025.
Copyright: © 2025 Yang, Zhang, Li, Wu, Sun, Yin, Fan and Li. 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:
Huizhen Yang, Shanxi Agricultural University, Jinzhong, China
Hongquan Li, Shanxi Agricultural University, Jinzhong, China
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