ArticleBioengineered2021
Effect of sodium butyrate regulating IRAK1 (interleukin-1 receptor-associated kinase 1) on visceral hypersensitivity in irritable bowel syndrome and its mechanism.
Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Effect of microencapsulated sodium butyrate on abdominal symptoms and carbohydrate metabolism in patients with type 2 diabetes: a randomized placebo-controlled trial.Scientific reports · 2026Trial
- Article
- Efficacy and Safety of a Mixture of Microencapsulated Sodium Butyrate, Probiotics, and Short Chain Fructooligosaccharides in Patients with Irritable Bowel Syndrome-A Randomized, Double-Blind, Placebo-Controlled Study.Journal of clinical medicine · 2024Article
- Potential Therapeutic Effects of Short-Chain Fatty Acids on Chronic Pain.Current neuropharmacology · 2024Review
- New insights into irritable bowel syndrome pathophysiological mechanisms: contribution of epigenetics.Journal of gastroenterology · 2023Review
- Peptide YY 3-36 attenuates trinitrobenzene sulfonic acid-induced colitis in mice by modulating Th1/Th2 differentiation.Bioengineered · 2022Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The current study aimed to investigate the effects of sodium butyrate on the level of colonic protein IRAK1 (interleukin-1 receptor-associated kinase 1) in irritable bowel syndrome (IBS) models as well as revealing the relationship between IRAKI level and visceral sensitivity during the progression of IBS. IBS symptoms were induced using TNBS (2,4,6-trinitrobenzene sulfonic acid) in mice and using IL-33 in HT-29 cells, which were then hanlded with sodium butyrate (100 mM for each mice and 0.05 M for HT-29 cells). The threshold of visceral pain and the expression of IRAKI in mice, and the level of IRAKI in HT-29 cells were detected. The data showed that the level of IRAK1 in IBS mice was higher than that in the control group, while the pre-treatment with sodium butyrate could solidy suppressed the level of IRAK1. Morevoer, it was found that the level of IRAK1 was negatively correlated with the pain threshold. In in vitro assays, the level of IRAK1 was firstly induced by IL-33 stimulation and then suppressed by sodium butyrate pretreatment. Collectively, the level of IRAKI showed an obvioulty positive relation with visceral hypersensitivity in IBS models, and the treatment with sodium butyrate could alleviate visceral hypersensitivity by inhibiting the expression of IRAKI.
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