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Improved colonic inflammation by nervonic acid via inhibition of NF-κB signaling pathway of DSS-induced colitis mice.

Authors :
Yuan SN
Wang MX
Han JL
Feng CY
Wang M
Wang M
Sun JY
Li NY
Simal-Gandara J
Liu C
Source :
Phytomedicine : international journal of phytotherapy and phytopharmacology [Phytomedicine] 2023 Apr; Vol. 112, pp. 154702. Date of Electronic Publication: 2023 Feb 04.
Publication Year :
2023

Abstract

Background: Nervonic acid (C24:1 <superscript>∆15</superscript> , 24:1 ω-9, cis-tetracos-15-enoic acid; NA), a long-chain monounsaturated fatty acid, plays an essential role in prevention of metabolic diseases, and immune regulation, and has anti-inflammatory properties. As a chronic, immune-mediated inflammatory disease, ulcerative colitis (UC) can affect the large intestine. The influences of NA on UC are largely unknown.<br />Purpose: The present study aimed to decipher the anti-UC effect of NA in the mouse colitis model. Specifically, we wanted to explore whether NA can regulate the levels of inflammatory factors in RAW264.7 cells and mouse colitis model.<br />Methods: To address the above issues, the RAW264.7 cell inflammation model was established by lipopolysaccharide (LPS), then the inflammatory factors tumor necrosis factor-α (TNF-α), Interleukin-6 (IL-6), Interleukin-1β (IL-1β), and Interleukin-10 (IL-10) were detected by Enzyme-linked immunosorbent assay (ELISA). The therapeutic effects of NA for UC were evaluated using C57BL/6 mice gavaged dextran sodium sulfate (DSS). Hematoxylin and eosin (H&E) staining, Myeloperoxidase (MPO) kit assay, ELISA, immunofluorescence assay, and LC-MS/MS were used to assess histological changes, MPO levels, inflammatory factors release, expression and distribution of intestinal tight junction (TJ) protein ZO-1, and metabolic pathways, respectively. The levels of proteins involved in the nuclear factor kappa-B (NF-κB) pathway in the UC were investigated by western blotting and RT-qPCR.<br />Results: In vitro experiments verified that NA could reduce inflammatory response and inhibit the activation of key signal pathways associated with inflammation in LPS-induced RAW264.7 cells. Further, results from the mouse colitis model suggested that NA could restore intestinal barrier function and suppress NF-κB signal pathways to ameliorate DSS-induced colitis. In addition, untargeted metabolomics analysis of NA protection against UC found that NA protected mice from colitis by regulating citrate cycle, amino acid metabolism, pyrimidine and purine metabolism.<br />Conclusion: These results suggested that NA could ameliorate the secretion of inflammatory factors, suppress the NF-κB signaling pathway, and protect the integrity of colon tissue, thereby having a novel role in prevention or treatment therapy for UC. This work for the first time indicated that NA might be a potential functional food ingredient for preventing and treating inflammatory bowel disease (IBD).<br />Competing Interests: Declaration of competing interest The authors declare that there are no financial conflicts of interest in regard to this work.<br /> (Copyright © 2023 The Author(s). Published by Elsevier GmbH.. All rights reserved.)

Details

Language :
English
ISSN :
1618-095X
Volume :
112
Database :
MEDLINE
Journal :
Phytomedicine : international journal of phytotherapy and phytopharmacology
Publication Type :
Academic Journal
Accession number :
36764096
Full Text :
https://doi.org/10.1016/j.phymed.2023.154702