Abstract：
Deoxynivalenol (DON) is a major mycotoxin present in staple foods (particularly in cereal products) that induces intestinal inflammation and disrupts intestinal integrity. Lactoferrin (LF) is a multifunctional protein that contributes to maintaining intestinal homeostasis and improving host health. However, the protective effects of LF on DON-induced intestinal dysfunction remain unclear.
This study aimed to investigate the effects of LF on DON-induced intestinal dysfunction in mice, and its underlying protective mechanism.
Male BALB/c mice (5 wk old) with similar body weights were divided into 4 groups (n = 6/group) and treated as follows for 5 wk: Veh [peroral vehicle daily, commercial (C) diet]; LF (peroral 10 mg LF/d, C diet); DON (Veh, C diet containing 12 mg DON/kg); and LF + DON (peroral 10 mg LF/d, DON diet). Intestinal morphology, tight junction proteins, cytokines, and microbial community were determined. Data were analyzed by 2-factor ANOVA or Kruskal-Wallis test.
The DON group exhibited lower final body weight (-12%), jejunal villus height (VH; -41%), and jejunal occludin expression (-36%), and higher plasma IL-1β concentration (+85%) and jejunal Il1b mRNA expression (+98%) compared with the Veh group (P < 0.05). In contrast, final body weight (+19%), jejunal VH (+49%), jejunal occludin (+53%), and intelectin 1 protein expression (+159%) were greater in LF + DON compared with DON (P < 0.05). Additionally, jejunal Il1b mRNA expression (-31%) and phosphorylation of p38 and extracellular signal regulated kinase 1/2 (-40% and - 38%) were lower in LF + DON compared with DON (P < 0.05). Furthermore, the relative abundance of Clostridium XIVa (+181%) and colonic butyrate concentration (+53%) were greater in LF + DON compared with DON (P < 0.05).
Our study highlights a promising antimycotoxin approach using LF to alleviate DON-induced intestinal dysfunction by modulating the mitogen-activated protein kinase pathway and gut microbial community in mice.
This study aimed to investigate the effects of LF on DON-induced intestinal dysfunction in mice, and its underlying protective mechanism.
Male BALB/c mice (5 wk old) with similar body weights were divided into 4 groups (n = 6/group) and treated as follows for 5 wk: Veh [peroral vehicle daily, commercial (C) diet]; LF (peroral 10 mg LF/d, C diet); DON (Veh, C diet containing 12 mg DON/kg); and LF + DON (peroral 10 mg LF/d, DON diet). Intestinal morphology, tight junction proteins, cytokines, and microbial community were determined. Data were analyzed by 2-factor ANOVA or Kruskal-Wallis test.
The DON group exhibited lower final body weight (-12%), jejunal villus height (VH; -41%), and jejunal occludin expression (-36%), and higher plasma IL-1β concentration (+85%) and jejunal Il1b mRNA expression (+98%) compared with the Veh group (P < 0.05). In contrast, final body weight (+19%), jejunal VH (+49%), jejunal occludin (+53%), and intelectin 1 protein expression (+159%) were greater in LF + DON compared with DON (P < 0.05). Additionally, jejunal Il1b mRNA expression (-31%) and phosphorylation of p38 and extracellular signal regulated kinase 1/2 (-40% and - 38%) were lower in LF + DON compared with DON (P < 0.05). Furthermore, the relative abundance of Clostridium XIVa (+181%) and colonic butyrate concentration (+53%) were greater in LF + DON compared with DON (P < 0.05).
Our study highlights a promising antimycotoxin approach using LF to alleviate DON-induced intestinal dysfunction by modulating the mitogen-activated protein kinase pathway and gut microbial community in mice.
摘要：
背景:脱氧雪腐镰刀菌烯醇(DON)是存在于主食(特别是谷物产品)中的主要霉菌毒素,其诱导肠道炎症并破坏肠道完整性。乳铁蛋白（LF）是一种多功能蛋白质，有助于维持肠道稳态和改善宿主健康。然而,LF对DON诱导的肠功能障碍的保护作用尚不清楚。
目的：本研究旨在探讨LF对DON诱导的小鼠肠功能障碍的影响。及其潜在的保护机制。
方法：将体重相似的雄性BALB/c小鼠（5周龄）分为4组（n=6/组），如下治疗5周：Veh[每日经口溶媒，商业（C）饮食]；LF（口服10mgLF/d，C饮食）；DON（VEH，含12mgDON/kg的C饮食）；和LF+DON（口服10mgLF/d，DON饮食）。肠道形态,紧密连接蛋白，细胞因子,并确定了微生物群落。通过2因素ANOVA或Kruskal-Wallis检验分析数据。
结果：DON组的最终体重较低（-12％），空肠绒毛高度（VH；-41%），和空肠闭塞蛋白表达（-36％），与Veh组相比，血浆IL-1β浓度（85％）和空肠Il1bmRNA表达（98％）更高（P<0.05）。相比之下,最终体重（+19%），空肠VH(+49%),空肠闭塞蛋白(+53%),与DON相比，LFDON和intelectin1蛋白表达（159％）更高（P<0.05）。此外,与DON相比，LFDON中空肠Il1bmRNA表达（-31％），p38和细胞外信号调节激酶1/2的磷酸化（-40％和-38％）较低（P<0.05）。此外，与DON相比，LFDON中XIVa梭菌的相对丰度（181%）和结肠丁酸酯浓度（53%）更高（P<0.05）。
结论：我们的研究强调了一种有前景的抗霉菌毒素方法，使用LF通过调节小鼠的丝裂原活化蛋白激酶途径和肠道微生物群落来减轻DON诱导的肠功能障碍。
目的：本研究旨在探讨LF对DON诱导的小鼠肠功能障碍的影响。
方法：将体重相似的雄性BALB/c小鼠（5周龄）分为4组（n=6/组），如下治疗5周：Veh[每日经口溶媒，
结果：DON组的最终体重较低（-12％），
结论：我们的研究强调了一种有前景的抗霉菌毒素方法，使用LF通过调节小鼠的丝裂原活化蛋白激酶途径和肠道微生物群落来减轻DON诱导的肠功能障碍。
