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Sodium Decanoate Improves Intestinal Epithelial Barrier and Antioxidation via Activating G Protein-Coupled Receptor-43.

ABSTRACT: The study was conducted to explore actions of decanoic acid on regulating intestinal barrier and antioxidant functions in intestinal epithelium cells isolated from porcine jejunum (IPEC-J2) and C57/BL6 mice models. In vitro and vivo assays, mice and IPEC-J2 cells treated by H₂O₂ were disposed of sodium decanoate and sodium butyrate to determine intestinal barrier and antioxidant functions of the host. Results showed that sodium decanoate upregulated expression of tight junction proteins and improved antioxidant capacity in both IPEC-J2 cells treated by H₂O₂ and mice models (p < 0.05). Sodium decanoate increased weight gain and ileal villus height of mice compared with control and sodium butyrate treatments (p < 0.05). Sodium decanoate increased α-diversity of ileal microbiota, volatile fatty acids concentration, and G protein-coupled receptor-43 (GPR-43) expression in the ileum and colon of mice (p < 0.05). In conclusion, sodium decanoate improved antioxidant capacity, intestinal morphology, and gut physical barrier of intestinal epithelial cells, resulting in an increase growth performance of mice, which is mediated through activating GPR-43 signaling.

SUBMITTER: Zhao J

PROVIDER: S-EPMC8401944 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Intestinal barrier function defects and dysregulation of intestinal immune responses are two key contributory factors in the pathogenesis of ulcerative colitis (UC). Phenazine biosynthesis-like domain-containing protein (PBLD) was recently identified as a tumor suppressor in gastric cancer, hepatocellular carcinoma, and breast cancer; however, its role in UC remains unclear. Therefore, we analyzed colonic tissue samples from patients with UC and constructed specific intestinal epithelial PBLD-deficient (PBLDIEC-/-) mice to investigate the role of this protein in UC pathogenesis. We found that epithelial PBLD was decreased in patients with UC and was correlated with levels of tight junction (TJ) and inflammatory proteins. PBLDIEC-/- mice were more susceptible to dextran sulfate sodium (DSS)- and 2,4,6-trinitrobenzene sulfonic acid-induced colitis compared with wild-type (WT) mice. In DSS-induced colitis, PBLDIEC-/- mice had impaired intestinal barrier function and greater immune cell infiltration in colonic tissue than WT mice. Furthermore, TJ proteins were markedly reduced in PBLDIEC-/- mice compared with WT mice with colitis. Nuclear factor (NF)-κB activation was markedly elevated and resulted in higher expression levels of downstream effectors (C-C motif chemokine ligand 20, interleukin [IL]-1β, IL-6, and tumor necrosis factor [TNF]-α) in colonic epithelial cells isolated from PBLDIEC-/- mice than WT mice with colitis. PBLD overexpression in intestinal epithelial cells (IECs) consistently inhibited TNF-α/interferon-γ-induced intestinal barrier disruption and TNF-α-induced inflammatory responses via the suppression of NF-κB. In addition, IKK inhibition (IKK-16) rescued excessive inflammatory responses induced by TNF-α in PBLD knockdown FHC cells. Co-immunoprecipitation assays showed that PBLD may interact with IKKα and IKKβ, thus inhibiting NF-κB signaling, decreasing inflammatory mediator production, attenuating colonic inflammation, and improving intestinal barrier function. Modulating PBLD expression may provide a novel approach for treatment in patients with UC.

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Sodium Decanoate Improves Intestinal Epithelial Barrier and Antioxidation via Activating G Protein-Coupled Receptor-43.

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