中文摘要：脱氧雪腐镰刀菌烯醇（DON），全球最常见的霉菌毒素，给动物性食品生产造成经济损失。家畜中猪对DON最敏感，因其吸收快而肠道菌群解毒能力低。特别是DON能扰乱肠屏障，引起炎症反应，严重损伤猪肠组织。本文利用猪小肠上皮细胞体外培养模型，评估了几种霉菌毒素解毒剂，包括膨润土、酵母细胞壁成分和由矿物质、微生物和植物性物质组成的混合物，对DON损伤的肠屏障和炎性反应的作用。结果发现，3种解毒剂都能以剂量依赖方式减轻DON引起的体外肠屏障破坏，它们还通过下调丝裂原活化蛋白激酶和Egr-1，不同程度地抑制由DON引起的炎症趋化因子的表达。值得注意的是，混合型解毒剂在细胞水平上效果最好，而大量的膨润土也能抑制DON引起的炎性损伤。本研究中体外评估猪肠屏障完整性与炎症信号为饲料添加剂，如致病性霉菌毒素的解毒剂，提供了灵敏而简单的生物测定替代方法。
外文摘要：Deoxynivalenol (DON), the most prevalent mycotoxin worldwide, leads to economic losses for animal food production. Swine is a most sensitive domestic animal to DON due to rapid absorption and low detoxification by gut microbiota. Specifically, DON can severely damage pig intestinal tissue by disrupting the intestinal barrier and inducing inflammatory responses. We evaluated the effects of several mycotoxin detoxifiers including bentonites, yeast cell wall components, and mixture-typed detoxifier composed of mineral, microorganisms, and phytogenic substances on DON-insulted intestinal barrier and pro-inflammatory responses using in vitro porcine enterocyte culture model. DON-induced disruption of the in vitro gut barrier was attenuated by all three mycotoxin detoxifiers in dose-dependent manners. These mycotoxin detoxifiers also suppressed DON-induced pro-inflammatory chemokine expression to different degrees, which was mediated by downregulation of mitogen-activated kinases and early growth response-1. Of note, the mixture-typed detoxifier was the most prominent mitigating agent at the cellular levels whereas the high dose of bentonite clay also had suppressive action against DON-induced pro-inflammatory insult. The in vitro porcine enterocyte-based assessment of intestinal barrier integrity and inflammatory signals provides sensitive and simplified alternative bioassay of feed additives such as detoxifiers against enteropathogenic mycotoxins with comprehensive mechanistic confirmation.
外文关键词：Mycotoxin detoxifiers；Porcine enterocytes；Deoxynivalenol
作者：Park, SH；Kim, J；Kim, D；Moon, Y
作者单位：Pusan Natl Univ
期刊名称：TOXICOLOGY IN VITRO
期刊影响因子：3.338
出版年份：2017
出版刊次：2
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