ArticleNutrients2021
Effects of Dietary Oat Beta-Glucans on Colon Apoptosis and Autophagy through TLRs and Dectin-1 Signaling Pathways-Crohn's Disease Model Study.
Article in Nutrients, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Effects of Oats (Frontiers in nutrition · 2021Pooled it
- Targeting cell death in Crohn's disease: from mechanisms to medicines.Cell death discovery · 2026Review
- Dietary polysaccharides in the management of inflammatory bowel disease: recent advances.Frontiers in nutrition · 2026Review
- Health benefits of oat dietary fibre in inflammatory bowel disease: a systematic review.Przeglad gastroenterologiczny · 2026Review
- The role of glycan-lectin interactions in the tumor microenvironment: immunosuppression regulators of colorectal cancer.American journal of cancer research · 2025Review
- Article
- Preparation, characterization and antioxidant and anticancerous potential of Quercetin loaded β-glucan particles derived from mushroom and yeast.Scientific reports · 2024Article
- Article
- Review
- Effect of vitamin DVeterinarni medicina · 2024Article
- Perspectives in the Application of High, Medium, and Low Molecular Weight OatFoods (Basel, Switzerland) · 2023Review
- Colon Expression of Chemokines and Their Receptors Depending on the Stage ofInternational journal of molecular sciences · 2022Article
- Beta-Glucan in Foods and Health Benefits.Nutrients · 2021Article
- Anti-Inflammatory Activity of Oat Beta-Glucans in a Crohn's Disease Model: Time- and Molar Mass-Dependent Effects.International journal of molecular sciences · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundCrohn's disease (CD) is characterized by chronic inflammation of the gastrointestinal tract with alternating periods of exacerbation and remission. The aim of this study was to determine the time-dependent effects of dietary oat beta-glucans on colon apoptosis and autophagy in the CD rat model.
methodsA total of 150 Sprague-Dawley rats were divided into two main groups: healthy control (H) and a TNBS (2,4,6-trinitrobenzosulfonic acid)-induced colitis (C) group, both including subgroups fed with feed without beta-glucans (βG-) or feed supplemented with low- (βGl) or high-molar-mass oat beta-glucans (βGh) for 3, 7, or 21 days. The expression of autophagy (LC3B) and apoptosis (Caspase-3) markers, as well as Toll-like (TLRs) and Dectin-1 receptors, in the colon epithelial cells, was determined using immunohistochemistry and Western blot.
resultsThe results showed that in rats with colitis, after 3 days of induction of inflammation, the expression of Caspase-3 and LC3B in intestinal epithelial cells did not change, while that of TLR 4 and Dectin-1 decreased. Beta-glucan supplementation caused an increase in the expression of TLR 5 and Dectin-1 with no changes in the expression of Caspase-3 and LC3B. After 7 days, a high expression of Caspase-3 was observed in the colitis-induced animals without any changes in the expression of LC3B and TLRs, and simultaneously, a decrease in Dectin-1 expression was observed. The consumption of feed with βGl or βGh resulted in a decrease in Caspase-3 expression and an increase in TLR 5 expression in the CβGl group, with no change in the expression of LC3B and TLR 4. After 21 days, the expression of Caspase-3 and TLRs was not changed by colitis, while that of LC3B and Dectin-1 was decreased. Feed supplementation with βGh resulted in an increase in the expression of both Caspase-3 and LC3B, while the consumption of feed with βGh and βGl increased Dectin-1 expression. However, regardless of the type of nutritional intervention, the expression of TLRs did not change after 21 days.
conclusionsDietary intake of βGl and βGh significantly reduced colitis by time-dependent modification of autophagy and apoptosis, with βGI exhibiting a stronger effect on apoptosis and βGh on autophagy. The mechanism of this action may be based on the activation of TLRs and Dectin-1 receptor and depends on the period of exacerbation or remission of CD.
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