Role of tumor necrosis factor-α and interleukin-1β in anorexia induction following oral exposure to the trichothecene deoxynivalenol (vomitoxin) in the mouse.
Role of tumor necrosis factor-α and interleukin-1β in anorexia induction following oral exposure to the trichothecene deoxynivalenol (vomitoxin) in the mouse.
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DOI：
10.2131/jts.39.875
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发表时间：
2014-12
期刊：
影响因子：
--
通讯作者：
Wenda Wu;Haibin Zhang
中科院分区：
文献类型：
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作者：
Wenda Wu;Haibin Zhang
脱氧雪腐镰刀菌烯醇（DON）是一种存在于谷物食品中的食源性真菌毒素，与人类和动物食物中毒有关。虽然厌食症的诱导已被描述为许多动物种属中DON诱导毒性的标志，但这种不良反应的机制基础尚未完全了解。本研究的目的是确定两种促炎细胞因子肿瘤坏死因子-α（TNF-α）和白细胞介素-1 β（IL-1β）在DON诱导的厌食症中的作用。在小鼠夜间摄食模型中，DON诱导的厌食反应在1小时发生并持续长达6小时。经口暴露于5 mg/kg bw的DON刺激脾脏和肝脏TNF-α和IL-1β的mRNA和血浆蛋白升高，这与厌食诱导相对应。TNF-α受体（TNFR）拮抗剂R-7050预处理可剂量依赖性地减轻TNF-α和DON诱导的厌食症。而IL-1受体1（IL-1 R1）拮抗剂IL-1 RA剂量依赖性地减轻IL-1β和DON诱导的厌食。总之，结果表明，TNF-α和IL-1β在口服暴露于DON后的厌食诱导中起贡献作用。
The trichothecene deoxynivalenol (DON), a foodborne mycotoxin found in grain-based foods, has been associated with human and animal food poisoning. Although induction of anorexia has been described as a hallmark of DON-induced toxicity in many animal species, the mechanistic basis for this adverse effect is not fully understood. The purpose of this research was to determine the role of two proinflammatory cytokines, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in DON-induced anorexia. In a nocturnal mouse food consumption model, DON-induced anorectic response occurred at 1 hr and lasted up to 6 hr. Similar anorectic effects were observed following acute administration of exogenous TNF-α and IL-1β. Oral exposure to DON at 5 mg/kg bw stimulated splenic and hepatic mRNA and plasma protein elevations of TNF-α and IL-1β that corresponded to anorexia induction. Pretreatment with the TNF-α receptor (TNFR) antagonist R-7050 dose-dependently attenuated both TNF-α- and DON-induced anorexia. While, the type 1 IL-1 receptor (IL-1R1) antagonist IL-1RA dose-dependently attenuated both IL-1β- and DON-induced anorexia. Taken together, the results suggest that both TNF-α and IL-1β play contributory role in anorexia induction following oral exposure to DON.