Beneficial Effects of Oat Beta-Glucan Dietary Supplementation in Colitis Depend on Its Molecular Weight
<p>Mean daily feed intake during three weeks of experiments. The data are presented as mean ± SE. Symbol * represents results significantly different from control conditions (HβG−): * <span class="html-italic">p</span> < 0.05, *** <span class="html-italic">p</span> < 0.001; symbol • represents significant differences between CβGl+ and CβGh+ groups: • <span class="html-italic">p</span> < 0.05; symbol ◊◊◊ represents significant differences between healthy (H) and control (C) rats within the same dietary intervention (HβGl+ vs. CβGl+): ◊◊◊ <span class="html-italic">p</span> < 0.001.</p> "> Figure 2
<p>Body weight gain curves of colitis [C] and healthy control [H] groups during three weeks of experiments.</p> "> Figure 3
<p>Macroscopic (left side) and microscopic (right side) changes in the colon caused by inflammation. <b>A1</b> and <b>A2</b>—CβG− group; <b>B1</b> and <b>B2</b>—CβGh+ group; <b>C1</b> and <b>C2</b>—CβGl+ group; <b>D1</b> and <b>D2</b>—HCβG− group. White arrows indicate diffuse multifocal inflammations (lymphocytes infiltration) of the submucosa of varying severity.</p> "> Figure 4
<p>Score of macroscopic damages in the mucosa and submucosa of the colon (mean ± SE).</p> "> Figure 5
<p>Score of microscopic damages in the mucosa and submucosa of the colon (mean ± SE).</p> "> Figure 6
<p>Percentage of (<b>a</b>) CD3 cells (lymphocyte T total), (<b>b</b>) CD8a+ cells (Tc lymphocytes), (<b>c</b>) CD4+ cells (Th lymphocytes), (<b>d</b>) CD45RA+ cells (B lymphocytes), and (<b>e</b>) CD161a+ cells (NK cells) in the intraepithelial lymphocytes (IEL) population (dithiothreitol, or DTT fraction). Symbol * represents results significantly different from the control group (control healthy animals βG−) (* <span class="html-italic">p</span> < 0.05, ** <span class="html-italic">p</span> < 0.01, *** <span class="html-italic">p</span> < 0.001); symbol • represents significant differences between the colitis βGl+ and colitis βGh+ groups (• <span class="html-italic">p</span> < 0.05, •• <span class="html-italic">p</span> < 0.01); symbol ◊ represents results significantly different between the control healthy animals and colitis rats within the same dietary intervention (healthy animals βGl+ vs. colitis βGl+) (◊ <span class="html-italic">p</span> < 0.05, ◊◊ <span class="html-italic">p</span> < 0.01, ◊◊◊ <span class="html-italic">p</span> < 0.001); (two-way ANOVA with Tukey post-hoc test); the data are presented as mean ± SE (<span class="html-italic">n</span> = 9).</p> "> Figure 6 Cont.
<p>Percentage of (<b>a</b>) CD3 cells (lymphocyte T total), (<b>b</b>) CD8a+ cells (Tc lymphocytes), (<b>c</b>) CD4+ cells (Th lymphocytes), (<b>d</b>) CD45RA+ cells (B lymphocytes), and (<b>e</b>) CD161a+ cells (NK cells) in the intraepithelial lymphocytes (IEL) population (dithiothreitol, or DTT fraction). Symbol * represents results significantly different from the control group (control healthy animals βG−) (* <span class="html-italic">p</span> < 0.05, ** <span class="html-italic">p</span> < 0.01, *** <span class="html-italic">p</span> < 0.001); symbol • represents significant differences between the colitis βGl+ and colitis βGh+ groups (• <span class="html-italic">p</span> < 0.05, •• <span class="html-italic">p</span> < 0.01); symbol ◊ represents results significantly different between the control healthy animals and colitis rats within the same dietary intervention (healthy animals βGl+ vs. colitis βGl+) (◊ <span class="html-italic">p</span> < 0.05, ◊◊ <span class="html-italic">p</span> < 0.01, ◊◊◊ <span class="html-italic">p</span> < 0.001); (two-way ANOVA with Tukey post-hoc test); the data are presented as mean ± SE (<span class="html-italic">n</span> = 9).</p> "> Figure 7
<p>Percentage of (<b>a</b>) CD3 cells (lymphocyte T total), (<b>b</b>) CD8a+ cells (Tc lymphocytes), (<b>c</b>) CD4+ cells (Th lymphocytes), (<b>d</b>) CD45RA+ cells (B lymphocytes), and (<b>e</b>) CD161a+ cells (NK cells) in the lamina propria lymphocytes (LPL) population (collagenase fraction); symbol * represents results significantly different from the control group (control healthy animals βG−) (* <span class="html-italic">p</span> < 0.05, ** <span class="html-italic">p</span> < 0.01, *** <span class="html-italic">p</span> < 0.001); symbol • represents significant differences between the colitis βGl+ and colitis βGh+ groups (• <span class="html-italic">p</span> < 0,05, •• <span class="html-italic">p</span> < 0.01, ••• <span class="html-italic">p</span> < 0.001); symbol ◊ represents results significantly different between the control healthy animals and colitis rats within the same dietary intervention (healthy animals βGl+ vs. colitis βGl+) (◊◊◊ <span class="html-italic">p</span> < 0.001); (two-way ANOVA with Tukey post-hoc test). The data are presented as mean ± SE (<span class="html-italic">n</span> = 9).</p> "> Figure 7 Cont.
<p>Percentage of (<b>a</b>) CD3 cells (lymphocyte T total), (<b>b</b>) CD8a+ cells (Tc lymphocytes), (<b>c</b>) CD4+ cells (Th lymphocytes), (<b>d</b>) CD45RA+ cells (B lymphocytes), and (<b>e</b>) CD161a+ cells (NK cells) in the lamina propria lymphocytes (LPL) population (collagenase fraction); symbol * represents results significantly different from the control group (control healthy animals βG−) (* <span class="html-italic">p</span> < 0.05, ** <span class="html-italic">p</span> < 0.01, *** <span class="html-italic">p</span> < 0.001); symbol • represents significant differences between the colitis βGl+ and colitis βGh+ groups (• <span class="html-italic">p</span> < 0,05, •• <span class="html-italic">p</span> < 0.01, ••• <span class="html-italic">p</span> < 0.001); symbol ◊ represents results significantly different between the control healthy animals and colitis rats within the same dietary intervention (healthy animals βGl+ vs. colitis βGl+) (◊◊◊ <span class="html-italic">p</span> < 0.001); (two-way ANOVA with Tukey post-hoc test). The data are presented as mean ± SE (<span class="html-italic">n</span> = 9).</p> "> Figure 8
<p>Influence of beta-glucans on the (<b>a</b>) C-reactive protein (CRP; (<b>b</b>) interleukin 12 (IL-12); (<b>c</b>) tumor necrosis factor α (TNF-α); (<b>d</b>) interleukin 1 (IL-1); and (<b>e</b>) interleukin 6 (IL-6) protein level; symbol * represents results significantly different from the control group (contro healthy animals βG−) (* <span class="html-italic">p</span> < 0.05, *** <span class="html-italic">p</span> < 0.001); symbol • represents significant differences between the colitis βGl+ and colitis βGh+ groups (• <span class="html-italic">p</span> < 0,05, •• <span class="html-italic">p</span> < 0.01, ••• <span class="html-italic">p</span> < 0.001); symbol ◊ represents results significantly different between healthy and colitis rats within the same dietary intervention (healthy βGl+ vs. colitis βGl+) (◊ <span class="html-italic">p</span> < 0.05, ◊◊ <span class="html-italic">p</span> < 0.01, ◊◊◊ <span class="html-italic">p</span> < 0.001) (two-way ANOVA with Tukey post-hoc test). The data are presented as mean ± SE (<span class="html-italic">n</span> = 9).</p> "> Figure 9
<p>Influence of beta-glucans on the interleukin 10 (IL-10) protein level. Symbol * represents results significantly different from the control group (control healthy animals βG−) (*** <span class="html-italic">p</span> < 0.001); symbol • represents significant differences between the colitis βGl+ and colitis βGh+ groups (••• <span class="html-italic">p</span> < 0.001); symbol ◊ represents results significantly different between the healthy and colitis rats within the same dietary intervention (healthy animals βGl+ vs. colitis βGl+) (◊ <span class="html-italic">p</span> < 0.05) (two-way ANOVA with Tukey post-hoc test). The data are presented as mean ± SE (<span class="html-italic">n</span> = 9).</p> "> Figure 10
<p>Influence of beta-glucans on the (<b>a</b>) total cyclooxygenase (COX) activity; (<b>b</b>) tromboksan A2 (TXA2); (<b>c</b>) prostaglandin E2 (PGE2); and (<b>d</b>) myeloperoxidase (MPO) protein level. Symbol * represents results significantly different from the control group (control healthy animals βG−) (* <span class="html-italic">p</span> < 0.05, *** <span class="html-italic">p</span> < 0.001); symbol • represents significant differences between the colitis βGl+ and colitis βGh+ groups (•• <span class="html-italic">p</span> < 0.01, ••• <span class="html-italic">p</span> < 0.001); symbol ◊ represents results significantly different between the healthy and colitis rats within the same dietary intervention (healthy animals βGl+ vs. colitis βGl+) (◊◊ <span class="html-italic">p</span> < 0.01, ◊◊◊ <span class="html-italic">p</span> < 0.001) (two-way ANOVA with Tukey post-hoc test). The data are presented as mean ± SE (<span class="html-italic">n</span> = 9).</p> "> Figure 10 Cont.
<p>Influence of beta-glucans on the (<b>a</b>) total cyclooxygenase (COX) activity; (<b>b</b>) tromboksan A2 (TXA2); (<b>c</b>) prostaglandin E2 (PGE2); and (<b>d</b>) myeloperoxidase (MPO) protein level. Symbol * represents results significantly different from the control group (control healthy animals βG−) (* <span class="html-italic">p</span> < 0.05, *** <span class="html-italic">p</span> < 0.001); symbol • represents significant differences between the colitis βGl+ and colitis βGh+ groups (•• <span class="html-italic">p</span> < 0.01, ••• <span class="html-italic">p</span> < 0.001); symbol ◊ represents results significantly different between the healthy and colitis rats within the same dietary intervention (healthy animals βGl+ vs. colitis βGl+) (◊◊ <span class="html-italic">p</span> < 0.01, ◊◊◊ <span class="html-italic">p</span> < 0.001) (two-way ANOVA with Tukey post-hoc test). The data are presented as mean ± SE (<span class="html-italic">n</span> = 9).</p> "> Figure 11
<p>Two-dimensional heat map showing all genes analyzed for each exposure combination, and representing the average gene expression levels. Genes that were up-regulated are shown in red, and genes that were down-regulated are shown in green in the experimental group: (<b>a</b>) in the CβG− group vs. HβG−; (<b>b</b>) in the CβGl+ group vs CβG−; (<b>c</b>) in the CβGh+ group vs CβG−.</p> ">
Abstract
:1. Introduction
2. Results
2.1. Feed Consumption and Body Weight Gain
2.2. Macroscopic and Microscopic Changes
2.3. Influence of Beta-Glucans on Intestinal Lymphocyte Subpopulations
2.4. Influence of Beta-Glucans on the Chosen Markers of Immunity
2.5. Selected Inflammatory Markers
2.6. Effect of Beta-Glucans on the Expression of Genes Encoding Inflammatory Cytokines and their Receptors
3. Discussion
4. Materials and Methods
4.1. Preparation and Characterization of Deproteinated Oat Beta-Glucan Fractions
4.2. Animal Treatment and Experimental Design
4.3. Tissue Collection and Preparation
4.4. Isolation of Lymphocytes from Colon Tissue
4.5. Phenotypic Analysis of the Isolated Leukocytes
4.6. Determination of Inflammation Parameters
4.7. RNA Isolation, Reverse Transcription, and Real-Time PCR
4.8. Statistical Analysis
5. Conclusions
Supplementary Materials
Author Contributions
Funding
Acknowledgments
Conflicts of Interest
References
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Sample Availability: Samples of the compounds are available from the authors. |
Experimental Feeds | H Group | C Group |
---|---|---|
Damage score (0–10) | ||
βG− | 0 (0) | 2,5 (2–4) |
βGl+ | 0 (0) | 1 (1–2) |
βGh+ | 0 (0) | 1 (1–2) |
Experimental Feeds | H Group | C Group |
---|---|---|
Damage score (0–6) | ||
βG− | 0 (0–1) | 2 (2–5) |
βGl+ | 0 (0–1) | 2 (1–2) |
βGh+ | 0 (0–1) | 2 (1–2) |
Nutrients in Feeds | Declared Composition | Analyzed Composition | ||||
---|---|---|---|---|---|---|
βGl+ | βGh+ | βG− | βG+ | βGh+ | βG− | |
Protein | 14.0 | 14.0 | 14.0 | 12.89 ± 1.80 | 12.49 ± 1.75 | 12.75 ± 1.78 |
Carbohydrates | 71.01 | 71.01 | 72.01 | 69.1 ± 2.3 | 68.1 ± 2.7 | 69.8 ± 2.7 |
Fat | 4.0 | 4.0 | 4.0 | 3.2 ± 0.1 | 3.3 ± 0.1 | 3.5 ± 0.8 |
Fiber | 5.0 | 5.0 | 5.0 | 3.7 ± 0.4 | 3.6 ± 0.4 | 3.5 ± 0.3 |
β-Glucans (%) | 1.0 | 1.0 | 0.0 | 0.91 ± 0.076 | 0.92 ± 0.388 | 0.0 |
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Żyła, E.; Dziendzikowska, K.; Gajewska, M.; Wilczak, J.; Harasym, J.; Gromadzka-Ostrowska, J. Beneficial Effects of Oat Beta-Glucan Dietary Supplementation in Colitis Depend on Its Molecular Weight. Molecules 2019, 24, 3591. https://doi.org/10.3390/molecules24193591
Żyła E, Dziendzikowska K, Gajewska M, Wilczak J, Harasym J, Gromadzka-Ostrowska J. Beneficial Effects of Oat Beta-Glucan Dietary Supplementation in Colitis Depend on Its Molecular Weight. Molecules. 2019; 24(19):3591. https://doi.org/10.3390/molecules24193591
Chicago/Turabian StyleŻyła, Ewa, Katarzyna Dziendzikowska, Małgorzata Gajewska, Jacek Wilczak, Joanna Harasym, and Joanna Gromadzka-Ostrowska. 2019. "Beneficial Effects of Oat Beta-Glucan Dietary Supplementation in Colitis Depend on Its Molecular Weight" Molecules 24, no. 19: 3591. https://doi.org/10.3390/molecules24193591