Glucuronolactone improves lung injury caused by PRRSV and DON co-challenge by enhancing the Nrf2-mediated antioxidant capacity in weaning piglets
文献类型: 外文期刊
作者: Hou, Jing 1 ; Cui, Chenbin 1 ; Wu, Jing 1 ; Tian, Min 1 ; Lu, Qi 1 ; Liu, Shilong 1 ; Ye, Guohao 1 ; Tian, Chaoyang 1 ; Tang, Jiaxi 1 ; Gao, Kaiguo 1 ; Wang, Li 1 ; Jiang, Zongyong 1 ; Qiu, Yueqin 1 ; Yang, Xuefen 1 ;
作者机构: 1.State Key Lab Swine & Poultry Breeding, Guangzhou 510640, Peoples R China
2.Minist Agr & Rural Affairs, Key Lab Anim Nutr & Feed Sci South China, Guangzhou 510640, Peoples R China
3.Guangdong Prov Key Lab Anim Breeding & Nutr, Guangzhou 510640, Peoples R China
4.Guangdong Acad Agr Sci, Inst Anim Sci, Guangzhou 510640, Peoples R China
关键词: Glucuronolactone; deoxynivalenol; PRRSV; oxidative stress; lung injury; Nrf2; piglets
期刊名称:VETERINARY RESEARCH ( 影响因子:3.5; 五年影响因子:4.0 )
ISSN: 0928-4249
年卷期: 2025 年 56 卷 1 期
页码:
收录情况: SCI
摘要: In the pig industry, both deoxynivalenol (DON) challenge and porcine reproductive and respiratory syndrome virus (PRRSV) infection can negatively impact the growth performance of pigs, thereby impairing the healthy development of the industry. Glucuronolactone (GLU) has been shown to be a potent antioxidant that helps alleviate oxidative stress. Therefore, this study aimed to investigate the effect of GLU on oxidative stress and lung injury induced by co-challenge with PRRSV and DON. Eighteen weaned piglets were randomly divided into three groups: control (CON), DON, and DON + GLU. After DON and/or GLU treatment for two weeks, all pigs were intramuscularly injected with PRRSV and treated with DON and/or GLU for another three weeks. Three weeks post-PRRSV infection, piglets in the DON group exhibited impaired growth performance, severe lung injury, and elevated viral loads. By contrast, piglets in the DON + GLU group showed improved growth performance and lung health, as well as reduced viral loads. GLU also inhibited inflammation, excessive autophagy and apoptosis induced by PRRSV and DON co-challenge in both porcine lung and MARC-145 cells, as indicated by reduced expression of pro-inflammatory factors, autophagy marker LC3, and apoptosis-related markers. Importantly, GLU can promote the phosphorylation and nuclear import of Nrf2, thereby enhancing antioxidant capacity and alleviating oxidative stress induced by PRRSV and DON co-challenge. Nrf2 inhibitor ML385 abolished the protective effect of GLU on inflammation and oxidative stress triggered by PRRSV and DON co-challenge. These findings suggest that GLU could mitigate oxidative stress to alleviate lung injury induced by PRRSV and DON co-challenge via activating the Nrf2 pathway, highlighting its potential as a dietary supplement in the pig industry.
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