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dc.contributor.authorHu, Ping
dc.contributor.authorZong, Qiufang
dc.contributor.authorZhao, Yahui
dc.contributor.authorGu, Haotian
dc.contributor.authorLiu, YaYa
dc.contributor.authorGu, Fang
dc.contributor.authorLiu, Hao-Yu
dc.contributor.authorAhmed, Abdelkareem A
dc.contributor.authorBao, Wenbin
dc.contributor.authorCai, Demin
dc.date.accessioned2023-03-02T13:51:47Z
dc.date.available2023-03-02T13:51:47Z
dc.date.issued2022-11
dc.identifier.issn1541-6100
dc.identifier.urihttps://academic.oup.com/jn/article/152/11/2451/6687812
dc.identifier.urihttps://hdl.handle.net/13049/647
dc.descriptionJournal Articleen_US
dc.description.abstractBackground: 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. Objectives: This study aimed to investigate the effects of LF on DON-induced intestinal dysfunction in mice, and its underlying protective mechanism. Methods: 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. Results: 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). Conclusions: 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. J Nutr 2022;152:2451–2460en_US
dc.language.isoenen_US
dc.publisherOxford Academicen_US
dc.relation.ispartofseriesThe Journal of Nutrition;Vol. 152(11), 2451-2460.
dc.subjectDeoxynivalenoen_US
dc.subjectIntestinal dysfunctionen_US
dc.subjectLactoferrinen_US
dc.subjectMAPK pathwayen_US
dc.subjectGut microbial communityen_US
dc.titleLactoferrin Attenuates Intestinal Barrier Dysfunction and Inflammation by Modulating the MAPK Pathway and Gut Microbes in Miceen_US
dc.typeArticleen_US


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