Journal
RESEARCH IN VETERINARY SCIENCE
Volume 140, Issue -, Pages 18-25Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.rvsc.2021.08.004
Keywords
Platycodon grandiflorus polysaccharide; Pseudorabies virus; Autophagy; Replication; Akt; mTOR
Categories
Funding
- Shandong Natural Science Foundation of China [ZR2018MC027]
- Shandong Key RD Program [GG201809160113]
- National Nature Science Foundation of China [31872535]
- China Postdoctoral Science Foundation [2018M632704, 2019T120601]
- Funds of Shandong Double Tops Program
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The study showed that PGPSt can reduce PRV replication and inhibit PRV-induced autophagy. Additionally, PGPSt inhibits PRV replication by restoring the Akt/mTOR signaling pathway suppressed by PRV infection. These findings provide insights for the development of antiviral drugs.
Pseudorabies virus (PRV) is one of the common pathogens in farms. Platycodon grandiflorus polysaccharide (PGPS) has been reported with a variety of biological activities. Autophagy is one of the vital mechanisms for cells to cope with virus infection, and it may also inhibit or promote virus replication. This study was conducted to investigate the antiviral activity of total PGPS(PGPSt) against PRV and the role of virus-induced autophagy in the anti-PRV effect of PGPSt in PK-15 cells. First, we established an infection model and detected the autophagy induced by PRV in PK-15 cells. Then, the protective effect of PGPSt against PRV was evaluated, and the effect of PGPSt on PRV replication and virus-induced autophagy were analysed by quantitative polymerase chain reaction, enzyme-linked immunosorbent assay, Western blot and confocal immunofluorescence. Results showed that PGPSt can reduce the PRV replication. PRV infection resulted in the accumulation of autophagosomes, which were inhibited by PGPSt. Moreover, PGPSt upregulated the Akt/mammalian target of rapamycin (mTOR) signalling pathway repressed by PRV infection, whereas rapamycin attenuated the anti-PRV effect of PGPSt. These findings suggest that PGPSt possess a protective effect against PRV infection and can inhibit PRV replication through relieving PRV-induced autophagy. This article can provide ideas for the development of antiviral drugs.
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