Affiliation:
1. College of Life Sciences Longyan University Longyan China
2. Fujian Provincial Key Laboratory for the Prevention and Control of Animal Infectious Diseases and Biotechnology Longyan China
3. Key Laboratory of Preventive Veterinary Medicine and Biotechnology Longyan University Longyan China
Abstract
AbstractBackgroundPorcine reproductive and respiratory syndrome virus (PRRSV) infection causes severe inflammatory response, respiratory disease and sow reproductive failure. Quercetin is among the widely occurring polypheno found abundantly in nature. Quercetin has anti‐inflammatory, anti‐oxidative and anti‐viral properties.ObjectivesThis study aimed to explore the effect and mechanism of quercetin on PRRSV‐induced inflammation in MARC‐145 cells.MethodsObserving the cytopathic effect and measurements of inflammatory markers in MARC‐145 cells collectively demonstrate that quercetin elicits a curative effect on PRRSV‐induced inflammation. Liquid chromatography–mass spectrometry was further used for a non‐targeted metabolic analysis of the role of quercetin in the metabolic regulation of PRRSV inflammation in MARC‐145 cells.ResultsIt was shown that quercetin attenuated PRRSV‐induced cytopathy in MARC‐145 cells. Quercetin treatment inhibited PRRSV replication in MARC‐145 cells in a dose‐dependent manner. We also found that quercetin inhibited PRRSV‐induced mRNA expression and secretion levels of tumour necrosis factor‐α, interleukin 1β and interleukin 6. Metabolomics analysis revealed that quercetin ameliorated PRRSV‐induced inflammation. Pathway analysis results revealed that PRRSV‐induced pathways including arachidonic acid metabolism, linoleic acid, glycerophospholipid and alanine, aspartate and glutamate metabolism were suppressed by quercetin. Moreover, we confirmed that quercetin inhibited the activation of NF‐κB/p65 pathway, probably by attenuating PLA2, ALOX and COX mRNA expression.ConclusionsThese results provide a crucial insight into the molecular mechanism of quercetin in alleviating PRRSV‐induced inflammation.
Funder
National Natural Science Foundation of China
Natural Science Foundation of Fujian Province