Agriculture & Food, Volume 12, 2024

Streszczenie: Mycotoxins are fungal secondary metabolites, which threaten the lives of both animals and humans. The decontamination of cereal crops and fruits is almost impossible due to their physical and chemical stability. Zearalenone (ZEA) is a fusariotoxin that can cause hormonal, digestive, neurological or immune dysfunctions, pigs being one of the most affected species. Agro-industrial waste could be a viable solution to counteract the mycotoxins toxic effects as they are rich in bioactive compounds (polyphenols, polyunsaturated fatty acids etc) with anti-inflammatory, antioxidant and anti-microbial properties. Our results have shown that rapeseed meal could alleviate the proinflammatory effects induced by ZEA at the gut level. However, the mechanisms involved in this process are not known, therefore the aim of our ex vivo study was to investigate the signaling pathways responsible for the ability of rapeseed meal (unfermented-RSM or fermented with Saccharomyces cerevisiae-FRSM) to counteract the inflammatory response triggered by ZEA in porcine jejunum explants. The explants collected from the jejunum of healthy piglets were incubated in DMEM/F12 HAM medium and treated or not with ZEA 100µg/mL and with methanolic extracts of RSM/FRSM for 4 hours. Gene expression of a couple of signaling molecules involved in the innate immunity (TLR2, TLR4, TLR5, TLR9, MyD88, MD2) and inflammatory response (Nrf2, IRAK1, TRAF6, TAK1, TGFβ2, AP1, AKT), also of MAPKs (ERK1/2, JNK1/2, p38α) which regulates the activity of pro-inflammatory cytokines were evaluated. Our results showed that 100µg/mL of ZEA increased the gene expression of TAK1, TGFβ2, NF-κB, JNK2 and p38α MAPK. The main mechanism involved seems to be the activation of TLR4/MyD88/MD2 signaling pathway due to the up regulation of these gene expressions by ZEA. The addition of RSM/FRSM extracts was able to significantly reduce the effects of ZEA on the analyzed signaling molecules, to the control levels, mainly through the inhibition of the TLR4/MyD88/MD2 signaling pathway.