Ellagic Acid Alleviates Oxidative Stress by Mediating Nrf2 Signaling Pathways and Protects against Paraquat-Induced Intestinal Injury in Piglets

被引:51
作者
Xiao, Yuxin [1 ]
Huang, Rui [1 ]
Wang, Nan [1 ]
Deng, Yuankun [1 ]
Tan, Bie [1 ]
Yin, Yulong [1 ,2 ]
Qi, Ming [2 ,3 ]
Wang, Jing [1 ,4 ]
机构
[1] Hunan Agr Univ, Coll Anim Sci & Technol, Changsha 410128, Peoples R China
[2] Chinese Acad Sci, Natl Engn Lab Pollut Control & Waste Utilizat Liv, Lab Anim Nutr Physiol & Metab Proc, Key Lab Agroecol Proc Subtrop Reg,Inst Subtrop Ag, Changsha 410125, Peoples R China
[3] Univ Chinese Acad Sci, Coll Resources & Evironment, Beijing 100864, Peoples R China
[4] Hunan Normal Univ, Sch Life Sci, Hunan Prov Key Lab Anim Intestinal Funct & Regula, Anim Nutr & Human Hlth Lab, Changsha 410081, Peoples R China
基金
中国国家自然科学基金; 英国科研创新办公室; 中国博士后科学基金;
关键词
ellagic acid; intestinal barrier; Nrf2 signaling pathway; oxidative stress; piglets; MITOCHONDRIAL DYSFUNCTION; BARRIER DYSFUNCTION; POMEGRANATE JUICE; KAPPA-B; APOPTOSIS; PARAMETERS; CAPACITY; CELLS; SUPPLEMENTATION; ELLAGITANNINS;
D O I
10.3390/antiox11020252
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The gastrointestinal tract is a key source of superoxide so as to be one of the most vulnerable to oxidative stress damage. Ellagic acid (EA), a polyphenol displays widely biological activities owing to its strong antioxidant properties. Here, we investigated the protective benefits of EA on oxidative stress and intestinal barrier injury in paraquet (PQ)-challenged piglets. A total of 40 weaned piglets were randomly divided into five groups: Control, PQ, 0.005% EA-PQ, 0.01% EA-PQ, and 0.02% EA-PQ. Piglets were intraperitoneally injected with 4 mg/kg (BW) PQ or saline on d-18, and sacrificed on d-21 of experiment. EA treatments eliminated growth-check induced by PQ and increased serum superoxide dismutase (SOD) activity but decreased serum malondialdehyde (MDA) level as compared to PQ group. EA supplementation promoted Nrf2 nuclear translocation and enhanced heme oxygenase-1 (HO-1) and quinone oxidoreductase 1 (NQO1) protein abundances of small intestinal mucosa. Additionally, EA improved PQ-induced crypt deepening, goblet cells loss, and villi morphological damage. Consistently, EA increased tight junction protein expression as was evident from the decreased serum diamine oxidase (DAO) levels. EA could ameliorate the PQ-induced oxidative stress and intestinal damage through mediating Nrf2 signaling pathway. Intake of EA-rich food might prevent oxidative stress-mediated gut diseases.
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页数:15
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