Nontoxic dose of Phenethyl isothiocyanate ameliorates deoxynivalenol-induced cytotoxicity and inflammation in IPEC-J2 cells. (May 2021)

• Record Type: Journal Article
• Authors: Liu, Shuiping; Lin, Ziman; Mao, Xinru; Ge, Lei; Hou, Lili; Le, Guannan; Gan, Fang; Wen, Lixin; Huang, Kehe
• Is Part Of: Research in veterinary science. Volume 136(2021)
• Page Start: 66
• Page End: 73
• Publication Date: 2021-05
• Subjects: Phenethyl isothiocyanate -- Deoxynivalenol -- Inflammation -- IPEC-J2 cell -- NF-κB signal pathway; Veterinary medicine -- Periodicals; Veterinary Medicine -- Periodicals; Médecine vétérinaire -- Périodiques; Médecine vétérinaire -- Recherche -- Périodiques; Diergeneeskunde; 636.089
• DOI: 10.1016/j.rvsc.2021.02.002
• Languages: English
• ISSNs: 0034-5288

Abstract

Abstract: The intestinal tract is a target for the deoxynivalenol (DON), which has adverse effects in animals and humans' health by affecting intestinal functions. Phenethyl isothiocyanate (PEITC) is an important degradation product of glucosinolates (GSLs), belonging to an anti-nutritional factor that affects the digestion and absorption of nutrients in the animals' intestinal. However, little attention has been paid to the interaction and its mechanism between DON and PEITC. Therefore, the purpose of this study was to assess the effects of PEITC on DON-induced cytotoxicity and inflammation, and explore the potential mechanisms in IPEC-J2 cells. Our results showed that DON exposure could decrease the cell viability and pro-inflammatory cytokine expression in IPEC-J2 cells in a dose-dependent manner. PEITC treatment at the concentrations of 1.25–5 μM had no significant effect on IPEC-J2 cells viability, but above 10 μM of PEITC treatment significantly reduced the cell viability. Interestingly, 1.25–5 μM of PEITC treatment could suppress 4 μM of DON-induced decrease in cell viability and increase in pro-inflammatory cytokine expression. Meanwhile, the protein ratios of p-p65/p-65 and p-IκBα/IκBα were markedly decreased in the groups treated with 1.25–5 μM PEITC compared to DON exposure alone. However, the protective effects of PEITC treatment were significantly blocked after pre-treatment with LPS, NF-κB activator, in IPEC-J2 cells. In conclusion, these findings indicated that the nontoxic dose of PEITC could alleviate DON-induced cytotoxicity and inflammation responses via suppressing the NF-κB signaling pathway in IPEC-J2 cells. Our results provide a new theoretical basis for the rational addition of rapeseed meal in animal feedstuff. Highlights: PEITC treatment alleviated DON-induced cytotoxicity and inflammation via suppressing the NF-κB signaling pathway in IPEC-J2 cells.