ArticleJournal of cellular physiology2019
Regulation of ROS-NF-κB axis by tuna backbone derived peptide ameliorates inflammation in necrotizing enterocolitis.
Article in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- The Role of APOL1 in Necrotizing Enterocolitis and Its Promise as a Diagnostic Biomarker.Mediators of inflammation · 2026Article
- Intensive Value Utilization of Food-Derived Marine Immunoactive Peptides: Optimizing the Process Yield and Improving the Delivery Efficiency According to the Immune Activity Mechanism and Assisted Enzymatic Hydrolysis.Food science & nutrition · 2025Review
- Article
- New Insights into Antioxidant Peptides: An Overview of Efficient Screening, Evaluation Models, Molecular Mechanisms, and Applications.Antioxidants (Basel, Switzerland) · 2024Review
- Role of ferroptosis in the pathogenesis and as a therapeutic target of inflammatory bowel disease (Review).International journal of molecular medicine · 2023Review
- Spore Oil-Functionalized Selenium Nanoparticles Protect Pancreatic Beta Cells from Palmitic Acid-Induced Apoptosis via Inhibition of Oxidative Stress-Mediated Apoptotic Pathways.Antioxidants (Basel, Switzerland) · 2023Article
- Programmed death of intestinal epithelial cells in neonatal necrotizing enterocolitis: a mini-review.Frontiers in pediatrics · 2023Review
- Transient receptor potential melastatin 7 aggravates necrotizing enterocolitis by promoting an inflammatory response in children.Translational pediatrics · 2022Article
- Integrative analysis links ferroptosis to necrotizing enterocolitis and reveals the role ofiScience · 2022Article
- Mechanism of Neonatal Intestinal Injury Induced by Hyperoxia Therapy.Journal of immunology research · 2022Review
- Protective Effect of Tuna Bioactive Peptide on Dextran Sulfate Sodium-Induced Colitis in Mice.Marine drugs · 2021Article
- Differential Expression Profiles and Functional Prediction of circRNAs in Necrotizing Enterocolitis.BioMed research international · 2021Article
- Integrated analysis of a lncRNA‑mRNA network reveals a potential mechanism underlying necrotizing enterocolitis.Molecular medicine reports · 2020Article
- Isoprenaline protects intestinal stem cells from chemotherapy-induced damage.British journal of pharmacology · 2020Article
- Recent Advances in Prevention and Therapies for Clinical or Experimental Necrotizing Enterocolitis.Digestive diseases and sciences · 2019Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.