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Proteomic analysis reveals the antiviral effects of baicalin on pseudorabies virus. | LitMetric

Proteomic analysis reveals the antiviral effects of baicalin on pseudorabies virus.

Int J Biol Macromol

College of Veterinary Medicine, Jilin University, Changchun, China; Institute for Animal Health, Henan Academy of Agricultural Sciences, Key Laboratory of Animal Immunology of the Ministry of Agriculture, Zhengzhou, China; Jiangsu Co-Innovation Center for the Prevention and Control of Important Animal Infectious Disease and Zoonose, Yangzhou University, Nanjing, China. Electronic address:

Published: October 2024

AI Article Synopsis

  • Pseudorabies virus (PRV) is a major threat to livestock and humans, and this study investigates the effects of baicalin, a bioactive compound, on PRV infection.
  • Baicalin was found to effectively inhibit PRV by reducing the levels of 14 viral proteins related to the virus's ability to replicate and evade the immune system, as well as restoring 116 host proteins altered by the infection.
  • The study also reveals that baicalin influences various biological pathways, notably by reducing oxidative stress and activating the coagulation cascade, suggesting its potential as a therapeutic agent against PRV.

Article Abstract

Pseudorabies virus (PRV) poses a significant threat to livestock and even humans. Baicalin, a bioactive flavonoid glycoside with medicinal potential, has been reported to have various biological activities. However, its inhibitory effect on PRV remains poorly understood. In this study, we proved that baicalin effectively inhibits PRV infection. Proteomic analysis revealed that baicalin reduces the expression of 14 viral proteins, which are associated with virus replication, release and immune evasion. Furthermore, the abundance of 116 host proteins was altered by PRV infection, but restored to normal levels after treatment with baicalin. Pathway analysis indicated that baicalin mitigates reactive oxygen species (ROS) and suppresses abnormal mitochondrion by reducing the expression of NFU1 iron‑sulfur cluster scaffold homolog (NFU1) protein induced by PRV. Notably, baicalin also activates the complete coagulation cascade by increasing the expression of coagulation factor III (F3) protein and enhances nucleoplasm by upregulating the expression of solute carrier family 3 member 2 (SLC3A2) and CCAAT enhancer binding protein beta (CEBPB) proteins, contributing to its inhibitory effects on PRV. Our findings implied that baicalin has the potential to be developed as an anti-PRV drug and provide insights into the underlying molecular basis.

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Source
http://dx.doi.org/10.1016/j.ijbiomac.2024.134149DOI Listing

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