ArticleEuropean journal of medical research2024
Homocysteine aggravates intestinal inflammation through promotion of 5-LOX and COX-2 in IBD.
Article in European journal of medical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Colitis-associated colorectal carcinogenesis: molecular mechanisms and therapeutic potential.Molecular biomedicine · 2026Review
- MTHFR gene polymorphisms and their biochemical associations with serum vitamin D and IL-17 in ulcerative colitis.Journal of medical biochemistry · 2026Article
- Fecal microbiota transplantation plus immunotherapy in metastatic renal cell carcinoma: the phase 1 PERFORM trial.Nature medicine · 2026Article
- Anti-Inflammatory Effects of Lipoxin A4 inAnimals : an open access journal from MDPI · 2026Article
- Systemic strategies to prevent early diabetic retinopathy: targeting polyunsaturated fatty acid metabolism and eicosanoid signaling.Frontiers in medicine · 2026Review
- Multi-omics analyses reveal significant differences in the gut microbiota and metabolites in children with Kawasaki disease in Northwest China.Frontiers in immunology · 2026Article
- Integrated metabolomics and gut microbiota analyses reveal the protective effects of matrine in ulcerative colitis.Frontiers in chemistry · 2026Article
- Identification of ferroptosis-related genes in pediatric Crohn's disease using bioinformatics approaches.Scientific reports · 2025Article
- Colorectal Neoplasia Pathogenesis in Normal Appearing Colonic Mucosa -A Perspective With Focus on Eicosanoid Signaling Pathways.Cancer medicine · 2025Review
- KIF18A induces the EMT process of hepatoma cells through the 5-LOX-dependent arachidonic acid pathway.PloS one · 2025Article
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6 authors.
Funding
Abstract
backgroundHomocysteine (Hcy) is a pro-inflammatory molecule that has the potential to induce oxidative damage to cells and stimulate the release of inflammatory mediators. Hcy has been observed to enhance the production of inflammatory agents in vascular endothelial cells. However, the impact of Hcy on intestinal mucosal inflammation remains largely unexplored. Therefore, the objective of this study was to examine the potential of Hcy to stimulate the synthesis of inflammatory mediators and elucidate the underlying mechanisms in the intestinal mucosa.
methodsA total of 99 patients diagnosed with inflammatory bowel disease (IBD) and 10 healthy individuals were included in this study to assess the impact of homocysteine (Hcy) on the levels of leukotriene E4 (LTE4) and prostaglandin E2 (PGE2). The underlying mechanism responsible for the generation of LTE4 and PGE2 induced by Hcy was investigated using colitis rats and Caco-2 cells. 32 Sprague-Dawley rats were categorized into four groups: normal control, TNBS model, normal with Hcy injection, and TNBS model with Hcy injection. The mRNA expressions of 5-LOX, COX-2, and NF-κB were assessed using reverse transcription quantitative polymerase chain reaction (RT-qPCR). Caco-2 cells were subjected to treatment with varying concentrations (10, 20, 50, 100 μmol/L) of Hcy and incubated for different durations (1, 3, 6 h). The alterations in NF-κB activity, as well as the levels of Hcy, LTE4, and PGE2, were measured using enzyme-linked immunosorbent assay (ELISA).
resultsThe excretion of Hcy, LTE4, and PGE2 in urine exhibited significant increases in patients with inflammatory bowel disease (IBD), Crohn's disease (CD), and ulcerative colitis (UC). In addition, Hcy demonstrated a significant increase in the expression of 5-LOX, COX-2, and NF-κB, as well as elevated levels of LTE4 and PGE2 in rats with colitis. Furthermore, Hcy was found to induce NF-κB activation and nuclear translocation, thereby contributing to the enhanced synthesis of LTE4 and PGE2 in Caco-2 cells.
conclusionsHcy was found to enhance the expression of 5-LOX and COX-2 by activating NF-κB, thereby augmenting the production of LTE4 and PGE2, which ultimately exacerbates colonic inflammation in individuals with inflammatory bowel disease (IBD).
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