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The application of bamboo by-products such as bamboo branches, chips to recycle and produce pressed bamboo pulp is an urgent task in Vietnam. It perfectly replaces natural wood with artificial wood embryos from bamboo powder, which has both economic benefits of reserving the source of raw materials, environmental protection... The paper presents a study of the influence of technological parameters on the water absorption and swelling thickness of pressed bamboo pulp plywood in order to ameliorate the quality of pressed bamboo pulp plywood in production of new materials for civil engineering with environmentally friendly bamboo wood pulp materials.

Feeding with 10% leucosaccharides for 3 weeks mitigated the development of adenine-induced chronic kidney disease in mice, as assessed by plasma urea, renal expression of inflammatory- and fibrosis-associated molecules, and colonic expression of tight junction proteins. Leucosaccharides are exopolysaccharides produced by Leuconostoc mesenteroides subsp. mesenteroides strain NTM048. Sequencing of 16S rRNA also revealed that leucosaccharides reverse the accumulation of Desulfovibrionaceae and Bifidobacterium and the loss of Akkermansia following exposure to adenine. Taken together, the data suggest that supplementation with leucosaccharides may effectively prevent or improve management of chronic kidney disease by restoring the microbiota and the integrity of colonic barriers.

The anti-inflammatory effect of Citrus kawachiensis peel powder was examined in a murine model of dextran sodium sulfate (DSS)-induced colitic mice. In addition to the whole powder, its ethanol extract rich in polyphenolic compounds and ethanol extraction residue rich in dietary fibers were used. The whole powder ameliorated the DSS-induced body weight loss (body weight changes on day 9, Control 108 ± 2, DSS 91 ± 4, DSS+whole peel powder 106 ± 1%, p < 0.05), colon shortening (colon length, Control 5.0 ± 0.1, DSS 3.9 ± 0.1, DSS+whole peel powder 4.7 ± 0.1 cm, p < 0.05), increased expression of pro-inflammatory cytokines (e.g., TNF-α, Control 1.0 ± 0.1, DSS 22.2 ± 5.8, DSS+whole peel powder 4.3 ± 1.5 arbitrary unit, p < 0.05), and decreased expression of colonic tight junctions (TJs) (e.g., occludin, Control 1.00 ± 0.07, DSS 0.21 ± 0.07, DSS+whole peel powder 0.70 ± 0.06 arbitrary unit, p < 0.05). The resolution of abnormalities barring the decreased expression of zonula occludens-2, junctional adhesion molecule-A, and claudin-7 by the extraction residue was comparable to that achieved using the powder (body weight change 107 ± 1%; colon length 4.7 ± 0.1 cm; TNF-α 4.1 ± 0.7; occludin 0.58 ± 0.06 arbitrary unit, p < 0.05). The ethanol extract alone did not have any influence on these abnormalities (body weight change 94 ± 2%; colon length 4.1 ± 0.1 cm; TNF-α 40.5 ± 9.0 arbitrary unit; occludin 0.18 ± 0.02 arbitrary unit, p < 0.05). The powder and ethanol extraction residue, but not ethanol extract, increased fecal acetic acid concentration (Control 4.9 ± 0.6, DSS 5.0 ± 0.9, DSS+whole peel powder 8.8 ± 1.8, DSS+ethanol extract 5.3 ± 0.8, DSS+ethanol extraction residue 12.5 ± 1.1 mmol/L, p < 0.05). Taken together, DFs in the ethanol extraction residue largely contributed to the peel powder-mediated reduction of TJ barrier defect and inflammation in colitic mice.

Short-chain fatty acids (SCFAs), such as acetate, propionate, and butyrate, play an important role in the maintenance of intestinal homeostasis. In the present study, anti-inflammatory effects of SCFAs were examined in human intestinal Caco-2 cells and mouse colonic cultures. Stimulation of Caco-2 cells with tumor necrosis factor (TNF)-α induced interleukin (IL)-8 (TNF-α, 17.1 ± 7.2 vs Control, 1.00 ± 0.26, P0.01) and IL-6 expression (TNF-α, 21.7 ± 10.0 vs Control, 1.00 ± 0.28, P0.01) through the activation of nuclear factor κB p65, spleen tyrosine kinase, and mitogen-activated protein kinase pathways. Pretreatment of cells with acetate (5 mM, IL-8 1.23 ± 0.40, IL-6 2.19 ± 0.92, P0.01 ), propionate (2.5 mM, IL-8 2.45 ± 2.10, IL-6 2.19 ± 0.92, P0.01), or butyrate (0.625 mM, IL-8 1.44 ± 0.70, IL-6 2.31 ± 0.32, P0.01) suppressed inflammatory responses induced by TNF-α. Pharmacological inhibition of monocarboxylate transporter (MCT)-1 attenuated the suppression of inflammatory signals by SCFAs. High expression levels of CXC motif chemokine ligand 2 (CXCL2, an IL-8 homologue, DSS, 31.7 ± 9.8 vs Control, 1.00 ± 0.70, P0.01) and IL-6 (DSS, 17.5 ± 7.2 vs Control, 1.00 ± 0.68, P0.01) were observed in BALB/c mouse colonic cultures exposed to dextran sodium sulfate, whereas treatments with mixtures of SCFAs decreased these elevated expression levels (CXCL2 4.14 ± 2.88, IL-6 0.58 ± 0.28, P0.01). Our results suggest that SCFAs transported by MCT-1 suppress TNF-α-induced inflammatory signaling in intestinal cells.

Background Chronic kidney disease (CKD) is a worldwide health problem. Although the pathogenesis of CKD is still unclear, recent studies suggest that systemic inflammation caused by a dysregulated microflora and an impaired intestinal barrier is involved in CKD development. Objective We investigated the effects of the fermentable dietary fibers (DFs), unmodified guar gum (GG), and partially hydrolyzed GG (PHGG) (i.e., substances with distinct viscosity characteristics) on CKD development, with a particular focus on colonic tight junction (TJ) barriers in mice. Methods Male 7-wk-old ICR mice were fed an AIN-93G diet that contained 0.25% adenine for 2 wk to induce CKD. Mice fed adenine were then divided into 3 groups and fed the unsupplemented diet (CKD) or a diet containing 10% PHGG (CKD+PHGG) or GG (CKD+GG) for 3 wk. Control (CON) mice were fed an AIN-93G diet without adenine throughout the 5-wk experiment. Plasma urea concentration; the colonic TJ proteins zonula occludens (ZO) 1, ZO2, occludin, junctional adhesion molecule A (JAMA), and claudin isoforms; renal inflammatory cytokines tumor necrosis factor α (Tnfa), interleukin (Il ) 1β (Il1b), and Il6; and cecal short-chain fatty acids (SCFAs) and microflora were analyzed. Results Compared with the CON, CKD+PHGG, and CKD+GG groups, the CKD group had a 2.2- to 4.4-fold higher plasma urea concentration and greater expression of inflammatory cytokine genes in the kidney, including Tnfa (4.4- to 48-fold), Il1b (4.6- to 56-fold), and Il6 (8.8- to 115-fold). The CON, CKD+PHGG, and CKD+GG groups had greater expression of colonic TJ proteins including ZO1 (2.9- to 3.7-fold), ZO2 (3.4- to 4.3-fold), occludin (3.0- to 3.3-fold), JAMA (4.4- to 5.4-fold), and claudin 7 (2.1- to 2.6-fold) and higher cecal SCFA (1.8- to 3.5-fold) and Lactobacillus (2.7- to 4.0-fold) concentrations than the CKD group. Conclusion Supplemental feeding with fermentable DFs, such as GG and PHGG, might be effective for the prevention or management of CKD by restoring colonic barrier integrity and microflora composition, as shown in mice.

cope : Direct regulation of intestinal inflammation by intact dietary fibers is still unclear. Here, the anti-inflammatory regulation by intact guar gum (GG) was investigated using mice and human intestinal Caco-2 cells. Methods and results : Administration of dextran sodium sulfate (DSS) increased myeloperoxidase activity and CXC motif chemokine ligand2 (an IL-8 homologue) expression in the small intestines of mice, while supplemental GG reduced these increases. Stimulation of Caco-2 cells with tumor necrosis factor (TNF)-α induced IL-8 expression through nuclear factor kappa B p65, spleen tyrosine kinase, and mitogen-activated protein kinases pathways. Pre-treatment of cells with GG reduced the TNF-α-induced IL-8 expression and cellular signaling. GG increased the suppressor of cytokine signaling (SOCS)-1 expression in Caco-2 cells, suggesting that this is one of the probable mechanisms involved in GG-mediated anti-inflammatory regulation. The anti-inflammatory regulation and SOCS-1 expression induced by GG were sensitive to neutralization of toll-like receptor (TLR)2 and dectin-1, and to inhibition of Janus kinase (JAK) and tyrosine kinase cSrc pathways. Finally, supplemental GG increased SOCS-1 expression in the small intestines of both DSS-administered and normal mice. Conclusion : Intact GG activates TLR2 and dectin-1, and increases SOCS-1 expression via JAK and cSrc pathways, resulting in anti-inflammatory regulation in intestinal epithelium. This article is protected by copyright. All rights reserved

Heat shock proteins (HSPs) protect intestinal epithelial cell function, integrity and viability against many forms of stress. We hypothesized that dietary fibers (DFs) in the diet may increase HSP expression, since DFs are known to exhibit beneficial effects on intestinal health. The present study investigated the regulation of intestinal HSP expression by DFs, particularly psyllium fiber. Feeding psyllium fiber for 5 d increased HSP25 expression, but not HSP32 and HSP70 expression in the jejunum, ileum, and colon of mice at both the protein and mRNA levels. The increases in HSP25 expression did not correlate with cecal organic acid production by microbial fermentation. The water-insoluble fraction of psyllium fiber largely contributed to the induction of HSP25 expression, but feeding with other water-insoluble DFs from beet, wheat, and oats failed to induce intestinal HSP25 expression. Although the water-holding capacity of psyllium fiber was much higher than those of the other water-insoluble DFs examined, the increase in HSP25 expression induced by feeding polycarbophil, which possesses a high water-holding capacity similar to that of psyllium fiber, was much lower than that induced by psyllium fiber. Finally, induction of malondialdehyde production by hydrogen peroxide, an oxidant, in the colon of mice fed psyllium fiber was lower than that in mice fed with the control diets. Taken together, feeding psyllium fiber, especially the water-insoluble fraction, increases intestinal HSP25 expression and suppresses oxidant-induced malondialdehyde production.

BACKGROUND Dietary fiber (DF) and its fermentation metabolites play an important role in establishing and maintaining intestinal health. OBJECTIVE This study investigated the effects of fermentable DF, guar gum (GG), and partially hydrolyzed GG (PHGG) on the epithelial tight junction (TJ) barrier and inflammation in a murine model of dextran sodium sulfate (DSS)-induced colitis. METHODS In Expt. 1, male, 7-wk-old BALB/c mice weighing ∼21 g were fed diets with 0%, 5%, and 10% GG for 12 d and administered distilled water with 2% DSS for 7 d beginning 5 d after the start of feeding. In Expt. 2, mice were provided diets with or without 10% PHGG and GG for 13 d and administered distilled water with 2% DSS for 8 d from 5 d after the start of feeding. In Expt. 3, mice were provided diets with or without 10% PHGG and GG for 14 d without DSS administration. Colitis score, colon TJ proteins, and fecal SCFA concentrations were analyzed. RESULTS In Expts. 1 and 2, the clinical score in the DSS group was ∼100% greater than that in the DSS+10% GG and PHGG groups on days 12 and 13 (P < 0.01). The DSS+10% GG and PHGG groups showed ∼110%, 60%, 120%, and 110% greater (P < 0.05) expression of occludin and claudin 3, 4, and 7, respectively, in the colon than did the DSS group. The DSS+10% GG and PHGG groups had greater total fecal SCFA concentrations (25.1 and 12.0 mmol/L) than did the DSS group (3.3 mmol/L) on day 9 (P < 0.01). TJ protein expression did not differ between groups in Expt. 3. CONCLUSION These findings suggest that microbial metabolites of PHGG and GG, and possibly SCFAs, reduce intestinal barrier defects and inflammation in colitic mice.

Aims Severe pulmonary arterial hypertension (PAH) is an incurable disease whose exact mechanisms remain unknown. However, growing evidence highlights the role of inflammation and endothelin (ET) signaling. The lack of reliable models makes it difficult to investigate the pathophysiology of this disease. Our aim was therefore to develop a mouse model of severe PAH closely mimicking the human condition to explore the role of interleukin-6 (IL-6), and ET signaling in advanced PAH progression. Main methods Young male SV129 mice received vascular endothelial growth factor receptor inhibitor (SU5416) three times a week and were exposed to hypoxia (10% O 2 ) for three weeks. Molecular analysis and histological assessment were examined using real-time PCR, Western blot and immunostaining, respectively. Key findings The developed murine model presented important characteristics of severe PAH in human: concentric neointimal wall thickening, plexogenic lesions, recruitment of macrophages, and distal arteriolar wall muscularization. We detected an increase of IL-6 production and a stronger macrophage recruitment in adventitia of remodeled arterioles developing plexogenic lesions. Moreover, ET-1 and ET receptor A were up-regulated in lung lysates and media of remodeled arterioles. Recombinant IL-6 stimulated the proliferation and regulated endothelial cells in increasing ET-1 and decreasing ET receptor B. Significance These data describe a murine model, which displays the most important features of human severe PAH. We assume that inflammation, particularly IL-6 regulating ET signaling, plays a crucial role in forming plexogenic lesions. This model is thus reliable and might be used for a better understanding of severe PAH progression and treatment.