Investigate the metabolic changes in intestinal diseases by employing a 1 H-NMR-based metabolomics approach on Caco-2 cells treated with cedrol.

Autor: Xu MR; Doctoral Program in Microbial Genomics, National Chung Hsing University and Academia Sinica, Taichung, Taiwan.; Department of Forestry, National Chung Hsing University, Taichung, Taiwan., Lin CH; Department of Forestry, National Chung Hsing University, Taichung, Taiwan., Wang CH; Special Crop and Metabolome Discipline Cluster, Academy Circle Economy, National Chung Hsing University, Taichung, Taiwan., Wang SY; Doctoral Program in Microbial Genomics, National Chung Hsing University and Academia Sinica, Taichung, Taiwan.; Department of Forestry, National Chung Hsing University, Taichung, Taiwan.; Special Crop and Metabolome Discipline Cluster, Academy Circle Economy, National Chung Hsing University, Taichung, Taiwan.; Agricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan.
Jazyk: angličtina
Zdroj: BioFactors (Oxford, England) [Biofactors] 2025 Jan-Feb; Vol. 51 (1), pp. e2132. Date of Electronic Publication: 2024 Oct 16.
DOI: 10.1002/biof.2132
Abstrakt: Mitochondrial dysfunction may precipitate intestinal dysfunction, while inflammatory bowel disease manifests as a chronic inflammatory ailment affecting the gastrointestinal tract. This condition disrupts the barrier function of the intestinal epithelium and alters metabolic products. Increasing mitochondrial adenosine triphosphate (ATP) synthesis in intestinal epithelial cells presents a promising avenue for colitis treatments. Nevertheless, the impact of cedrol on ATP and the intestinal barrier remains unexplored. Hence, this study is dedicated to examining the cedrol's protective effect on an inflammatory cocktail (IC)-induced intestinal epithelial barrier dysfunction in Caco-2 cells. The finding reveals that cedrol enhances ATP content and the transepithelial electrical resistance value in the intestinal epithelial barrier. Moreover, cedrol mitigates the IC-induced decrease in the messenger ribonucleic acid (mRNA) expression of tight junction proteins (ZO-1, Occludin, and Claudin-1), thereby ameliorating intestinal epithelial barrier dysfunction. Furthermore, nuclear magnetic resonance (NMR)-based metabolomic analysis indicated that IC-exposed Caco-2 cells are restored by cedrol treatments. Notably, cedrol elevates metabolites such as amino acids, thereby enhancing the intestinal barrier. In conclusion, cedrol alleviates IC-induced intestinal epithelial barrier dysfunction by promoting ATP-dependent proliferation of Caco-2 cells and bolstering amino acid levels to sustain tight junction messenger ribonucleic acid expression.
(© 2024 International Union of Biochemistry and Molecular Biology.)
Databáze: MEDLINE