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Ginsenoside Rg1 Suppresses Type 2 PRRSV Infection via NF-κB Signaling Pathway In Vitro, and Provides Partial Protection against HP-PRRSV in Piglet

Authors :
Heyou Yi
Ruting Zhong
Guihong Zhang
Chenxiao Qin
Yong-Jie Chen
Jun Ma
Zhiqing Yu
Mengkai Cai
Kegong Tian
Qi Li
Deng Qiwei
Yao Chen
Heng Wang
Yingfang Wei
Guan Liang
Xiaoliang Han
Source :
Viruses, Vol 11, Iss 11, p 1045 (2019), Viruses, Volume 11, Issue 11
Publication Year :
2019
Publisher :
MDPI AG, 2019.

Abstract

Porcine reproductive and respiratory syndrome virus (PRRSV) is a huge threat to the modern pig industry, and current vaccine prevention strategies could not provide full protection against it. Therefore, exploring new anti-PRRSV strategies is urgently needed. Ginsenoside Rg1, derived from ginseng and notoginseng, is shown to exert anti-inflammatory, neuronal apoptosis-suppressing and anti-oxidant effects. Here we demonstrate Rg1-inhibited PRRSV infection both in Marc-145 cells and porcine alveolar macrophages (PAMs) in a dose-dependent manner. Rg1 treatment affected multiple steps of the PRRSV lifecycle, including virus attachment, replication and release at concentrations of 10 or 50 &micro<br />M. Meanwhile, Rg1 exhibited broad inhibitory activities against Type 2 PRRSV, including highly pathogenic PRRSV (HP-PRRSV) XH-GD and JXA1, NADC-30-like strain HNLY and classical strain VR2332. Mechanistically, Rg1 reduced mRNA levels of the pro-inflammatory cytokines, including IL-1&beta<br />IL-8, IL-6 and TNF-&alpha<br />and decreased NF-&kappa<br />B signaling activation triggered by PRRSV infection. Furthermore, 4-week old piglets intramuscularly treated with Rg1 after being challenged with the HP-PRRSV JXA1 strain display moderate lung injury, decreased viral load in serum and tissues, and an improved survival rate. Collectively, our study provides research basis and supportive clinical data for using Ginsenoside Rg1 in PRRSV therapies in swine.

Details

Language :
English
ISSN :
19994915
Volume :
11
Issue :
11
Database :
OpenAIRE
Journal :
Viruses
Accession number :
edsair.doi.dedup.....8792ff18fb3a0d1be99b125957832e57