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Regulation of ROS–NF‐κB axis by tuna backbone derived peptide ameliorates inflammation in necrotizing enterocolitis
Author(s) -
Zhang Le,
Fan Jianfeng,
He Jingya,
Chen Wenjuan,
Jin Weilai,
Zhu Yuting,
Sun Haibing,
Li Yawen,
Shi Yingzuo,
Jing Yulei,
Wang Xiaolei,
Han Shuping,
Li Zhengying
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28133
Subject(s) - reactive oxygen species , intracellular , antioxidant , nf κb , necrotizing enterocolitis , inflammation , chemistry , proinflammatory cytokine , lipopolysaccharide , peptide , nfkb1 , transcription factor , microbiology and biotechnology , biochemistry , signal transduction , immunology , biology , medicine , gene
Necrotizing enterocolitis (NEC) is the most common life‐threatening gastrointestinal disease encountered in the premature infant. It has been shown that the intercellular reactive oxygen species (ROS) generation activated by lipopolysaccharide involved in the nuclear factor kappa B (NF‐κB) activation and pathogenesis of NEC. Here, we report that an antioxidant peptide from tuna backbone protein (APTBP) reduces the inflammatory cytokines transcription and release. APTBP directly scavenges the free radical through 1,1‐diphenyl‐2‐picrylhydrazyl (DPPH) and 2‐phenyl‐4,4,5,5‐tetramethylimidazoline‐1‐oxyl 3‐oxide (PTIO) assay. In addition, APTBP reduces the intracellular ROS level, exhibiting an antioxidant activity within cells. Remarkably, gavage with APTBP attenuates the phenotype of NEC in the mice model. Mechanically, the NF‐κB activation, together with the expression of inflammatory cytokines are decreased significantly when intracellular ROS are eliminated by APTBP. Therefore, our findings demonstrated that an antioxidant peptide, APTBP, ameliorates inflammation in NEC through attenuating ROS–NF‐κB axis.