دورية أكاديمية
JNK molecule is a toxic target for IPEC-J2 cell barrier damage induced by T-2 toxin
| العنوان: | JNK molecule is a toxic target for IPEC-J2 cell barrier damage induced by T-2 toxin |
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| المؤلفون: | Fengjuan Chen, Youshuang Wang, Yunhe Chen, Jiayan Fan, Cong Zhang, Xiuyuan He, Xu Yang |
| المصدر: | Ecotoxicology and Environmental Safety, Vol 263, Iss , Pp 115247- (2023) |
| بيانات النشر: | Elsevier, 2023. |
| سنة النشر: | 2023 |
| المجموعة: | LCC:Environmental pollution LCC:Environmental sciences |
| مصطلحات موضوعية: | T-2 toxin, JNK, Intestinal epithelial cells, Tight junction, Inflammation, Environmental pollution, TD172-193.5, Environmental sciences, GE1-350 |
| الوصف: | The most prevalent contaminated mycotoxin in feed and grain is T-2 toxin. The T-2 toxin's primary action target is the gut because it is the main organ of absorption. T-2 toxin can cause intestinal damage, but, few molecular mechanisms have been elucidated. It is important to discover the key pathways by which T-2 toxin causes enterotoxicity. In this research, IPEC-J2 cells are used as a cell model to investigate the function of the MAPK signaling pathway in T-2 toxin-induced intestinal epithelial cell damage. Throughout this research, T-2 toxin results in functional impairment in IPEC-J2 cells by reducing the TJ proteins Claudin, Occludin-1, ZO-1, N-cadherin, and CX-43 expression. T-2 toxin significantly reduced the survival of IPEC-J2 cells and increased LDH release in a dose-dependent way. T-2 toxin induced IPEC-J2 cell oxidative stress by raising ROS and MDA content, and mitochondrial damage was indicated by a decline in MMP and an increase in the opening degree of MPTP. T-2 toxin upregulated the expression of ERK, P38 and JNK, which triggered the MAPK signaling pathway. In addition, T-2 toxin caused IPEC-J2 cell inflammation responses reflected by increased the levels of inflammation-related factors IL-8, p65, P-p65 and IL-6, and down-regulated IL-10 expression level. Inhibition JNK molecule can ease IPEC-J2 cell functional impairment and inflammatory response. In conclusion, as a consequence of the T-2 toxin activating the JNK molecule, oxidative stress and mitochondrial damage are induced, which impair cellular inflammation. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 0147-6513 |
| Relation: | http://www.sciencedirect.com/science/article/pii/S0147651323007510; https://doaj.org/toc/0147-6513 |
| DOI: | 10.1016/j.ecoenv.2023.115247 |
| URL الوصول: | https://doaj.org/article/7896c88a0c034ea98176984a0577f600 |
| رقم الأكسشن: | edsdoj.7896c88a0c034ea98176984a0577f600 |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 01476513 |
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| DOI: | 10.1016/j.ecoenv.2023.115247 |