Dataset Information

Anti-inflammatory effects of mannanase-hydrolyzed copra meal in a porcine model of colitis.

ABSTRACT: We evaluated the anti-inflammatory activity of mannanase-hydrolyzed copra meal (MNB), including ?-1,4-mannobiose (67.8%), in a dextran sodium sulfate (DSS)-induced porcine model of intestinal inflammation. In the DSS-positive control (POS) and MNB treatment (MCM) groups, DSS was first administered to piglets via intragastric catheter for 5 days, followed by 5 days administration of saline or MCM. A negative control group (NEG) received a saline alternative to DSS and MNB. Inflammation was assessed by clinical signs, morphological and histological measurements, gut permeability and neutrophil infiltration. Local production of TNF-? and IL-6 were analyzed by ELISA, colonic and ileal inflammatory gene expressions were assessed by real time RT-PCR, and CD4+CD25+ cell populations were analyzed by flow cytometry. Crypt elongation and muscle thickness, D-mannitol gut permeation, colonic expression of the inflammatory mediators TNF-? and IL-6 and myeloperoxidase activity were significantly lower in the MCM group than in that of POS group. The mRNA levels of ileal IL-1?, IL-6, IL-17 and TNF-? were significantly lower following MCM treatment than with POS treatment.MNB exerts anti-inflammatory activity in vivo, suggesting that MNB is a novel therapeutic that may provide relief to human and animals suffering from intestinal inflammation.

SUBMITTER: Ibuki M

PROVIDER: S-EPMC4073332 | biostudies-literature | 2014 May

REPOSITORIES: biostudies-literature

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Anti-inflammatory effects of mannanase-hydrolyzed copra meal in a porcine model of colitis.

Ibuki Masahisa M Fukui Kensuke K Kanatani Hiroyuki H Mine Yoshinori Y

The Journal of veterinary medical science 20140116 5

We evaluated the anti-inflammatory activity of mannanase-hydrolyzed copra meal (MNB), including β-1,4-mannobiose (67.8%), in a dextran sodium sulfate (DSS)-induced porcine model of intestinal inflammation. In the DSS-positive control (POS) and MNB treatment (MCM) groups, DSS was first administered to piglets via intragastric catheter for 5 days, followed by 5 days administration of saline or MCM. A negative control group (NEG) received a saline alternative to DSS and MNB. Inflammation was assess ...[more]

PMID: 24430661

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Project description:A preliminary study investigated the impact of commercial feed dilution with copra meal (CM) or cassava leaf meal (CLM) and enzyme supplementation on broiler performance. Commercial feed alone (control) or diluted with CM and CLM at a concentration of 100 and 200 g/kg in the starter and finisher diets, respectively, was fed without and with Challenzyme 300A at a concentration of 300 g/tonne in 2 × 2 factorial arrangements with a control. Two hundred, 7-day-old male, Cobb 500 broiler chicks were randomly assigned to 5 diets containing 4 replicates of 10 birds each. There were no interaction or main effects (P > 0.05) on feed intake during either the starter or finisher phase. In the starter phase, feed-to-gain ratio (F:G) increased (P < 0.05) in the group fed with CM without enzyme. Enzyme supplementation restored F:G similar to the control. Diet dilution with CM or CLM had no effect (P > 0.05) on weight gain (WG) in the starter phase. Diluting the feed with CM or CLM without enzyme suppressed (P < 0.05) WG and F:G in the finisher phase, but enzyme supplementation restored the lost performances. There were no interaction or main effects (P > 0.05) on the carcass traits. Enzyme supplementation reduced (P < 0.05) feed cost per kilogram of carcass. Heavier ceca were observed in the group fed with dilution diets (P < 0.05). Enzyme supplementation reduced cecum weight in the group fed with CM (P < 0.05). The heaviest (P < 0.05) abdominal fat was recorded in the group fed with enzyme-supplemented CM diet, and the lightest (P < 0.05) abdominal fat was recorded in the group fed with CLM with enzyme. In the main effects, lighter (P < 0.05) liver, gizzard, and proventriculus were recorded in the group fed with control diet than in the group fed with the CLM diets, but the weight of these segments did not differ (P > 0.05) between the control and CM groups and between the fiber sources. The results suggest that dilution of commercial diet with CM or CLM may be a viable option for medium- and small-scale broiler production in the region. There is need for more research in the level of dilution, enzyme source, and concentration.

Project description:Evodiamine (Evo) is an alkaloid that can be extracted from the berry fruit Evodia rutaecarpa and has been reported to exert various pharmacological effects, such as antidiarrheal, antiemetic and antiulcer effects. In vivo, the potential effects of Evo were investigated in a mouse model of dextran sodium sulfate (DSS)‑induced ulcerative colitis (UC) and in adenomatous polyposis coli (Apc)MinC/Gpt C57BL/6 mice with colorectal cancer (CRC), where the latter harbours a point‑mutation in the Apc gene. Evo suppressed the degree of weight loss and colon shortening induced by DSS, decreased the disease activity index value and ameliorated the pathological alterations in the colon of mice with UC as examined via H&E staining of colon tissues. In addition, Evo decreased the number and size of colonic tumors in ApcMinC/Gpt mice. Proteomics (colon tissues), ELISA (colon tissues and serum) and western blotting (colon tissues) results revealed that Evo inhibited NF‑κB to mediate the levels of various cytokines, including, in the DSS‑induced UC model, IL‑1β, IL‑2, IL‑6, IL‑8, TNF‑α, IFN‑γ (ELISA of colon tissues and serum), NF‑κB, IKKα+β, IκBα, S100a9, TLR4 and MyD88 (western blotting of colon tissues), and, in the colorectal cancer model, IL‑1β, IL‑2, IL‑6, IL‑15, IL‑17, IL‑22, TNF‑α (ELISA of colon tissues and serum), NF‑κB, IKKα+β, IκBα and S100a9 (western blotting of colon tissues), to achieve its anti‑inflammatory and antitumor effects. In vitro, Evo also reduced the viability of the colon cancer cell line SW480, inhibited mitochondrial membrane potential (MMP detection), caused G2/M‑phase arrest (cell cycle detection) and suppressed the translocation of phosphorylated‑NF‑κB from the cytoplasm into the nucleus (immunofluorescence of p‑NF‑κB). Theoretical evidence (MD simulations) suggest that Evo may bind to the ordered domain (α‑helix) of NF‑κB to influence this protein. The protein secondary structure changes were analyzed by the cpptraj module in Amber. In addition, these data provide experimental evidence that Evo may be an effective agent for treating UC and CRC.

Project description:BACKGROUND: Ulcerative colitis is a chronic inflammatory disease and involves multiple etiological factors. Acetic acid (AA)-induced colitis is a reproducible and simple model, sharing many characteristics with human colitis. N-acetylcysteine (NAC) has been widely used as an antioxidant in vivo and in vitro. NAC can affect several signaling pathways involving in apoptosis, angiogenesis, cell growth and arrest, redox-regulated gene expression, and inflammatory response. Therefore, NAC may not only protect against the direct injurious effects of oxidants, but also beneficially alter inflammatory events in colitis. This study was conducted to investigate whether NAC could alleviate the AA-induced colitis in a porcine model. METHODS: Weaned piglets were used to investigate the effects of NAC on AA-induced colitis. Severity of colitis was evaluated by colon histomorphology measurements, histopathology scores, tissue myeloperoxidase activity, as well as concentrations of malondialdehyde and pro-inflammatory mediators in the plasma and colon. The protective role of NAC was assessed by measurements of antioxidant status, growth modulator, cell apoptosis, and tight junction proteins. Abundances of caspase-3 and claudin-1 proteins in colonic mucosae were determined by the Western blot method. Epidermal growth factor receptor, amphiregulin, tumor necrosis factor-alpha (TNF-?), and toll-like receptor 4 (TLR4) mRNA levels in colonic mucosae were quantified using the real-time fluorescent quantitative PCR. RESULTS: Compared with the control group, AA treatment increased (P?<?0.05) the histopathology scores, intraepithelial lymphocyte (IEL) numbers and density in the colon, myeloperoxidase activity, the concentrations of malondialdehyde and pro-inflammatory mediators in the plasma and colon, while reducing (P?<?0.05) goblet cell numbers and the protein/DNA ratio in the colonic mucosa. These adverse effects of AA were partially ameliorated (P?<?0.05) by dietary supplementation with NAC. In addition, NAC prevented the AA-induced increase in caspase-3 protein, while stimulating claudin-1 protein expression in the colonic mucosa. Moreover, NAC enhanced mRNA levels for epidermal growth factor and amphiregulin in the colonic mucosa. CONCLUSION: Dietary supplementation with NAC can alleviate AA-induced colitis in a porcine model through regulating anti-oxidative responses, cell apoptosis, and EGF gene expression.

Dataset Information

Anti-inflammatory effects of mannanase-hydrolyzed copra meal in a porcine model of colitis.

Publications

Anti-inflammatory effects of mannanase-hydrolyzed copra meal in a porcine model of colitis.

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