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1.
J Agric Food Chem ; 67(48): 13299-13306, 2019 Dec 04.
Artigo em Inglês | MEDLINE | ID: mdl-31674784

RESUMO

l-Arabinose is a monosaccharide extracted from plants or fibers, which is known to have a variety of functional properties. In this study, we aim to investigate whether l-arabinose could inhibit colitis by modulating gut microbiota. l-Arabinose was administered in mice daily in a dextran sodium sulfate (DSS)-induced colitis model. The histological analysis, disease index, and the expression of inflammatory genes were measured. 16S-rRNA sequence analysis was performed to investigate gut microbiota. Intriguingly, we found that l-arabinose could repress DSS-induced colitis and inhibit p38-/p65-dependent inflammation activation. Besides that, our data revealed that l-arabinose-modulated DSS-induced gut microbiota were disturbed. Additionally, the perturbed gut microbiota was responsible for the suppressive effects of l-arabinose on DSS-induced colitis treated with antibiotics. Lastly, Caco-2 cells were used to confirm the protective effects of l-arabinose in colitis or inflammatory bowel disease. As expected, the protein expression levels in Caco-2 cells of pro-inflammatory genes, which were treated with l-arabinose and incubated with or without tumor necrosis factor alpha. Our work suggested that l-arabinose exerts anti-inflammation effects in DSS-induced colitis. These beneficial effects have correlations with the composition, diversity, and abundance of the gut microbiota regulated by l-arabinose. l-Arabinose could be a remarkable candidate as a functional food or novel therapeutic strategy for intestinal health.


Assuntos
Arabinose/administração & dosagem , Colite/tratamento farmacológico , Colite/microbiologia , Microbioma Gastrointestinal/efeitos dos fármacos , Animais , Colite/induzido quimicamente , Colite/imunologia , Citocinas/genética , Citocinas/imunologia , Sulfato de Dextrana/efeitos adversos , Feminino , Humanos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Fator de Transcrição RelA/genética , Fator de Transcrição RelA/imunologia , Proteínas Quinases p38 Ativadas por Mitógeno/genética , Proteínas Quinases p38 Ativadas por Mitógeno/imunologia
2.
J Agric Food Chem ; 67(48): 13282-13298, 2019 Dec 04.
Artigo em Inglês | MEDLINE | ID: mdl-31690068

RESUMO

Dietary supplementation with conjugated linoleic acid (CLA) has been reported to alleviate the effect of colitis in mice, but the mechanisms involved need further exploration. The study aimed to investigate how orally administered CLA alleviates dextran sulfate sodium (DSS)-induced colitis in mice. CLA was administered in five different doses: 40, 20, 10, 5, and 2.5 mg/day. Doses of CLA at 10 mg/day and higher alleviated colitis symptoms and reduced inflammation induced by DSS, in which 40, 20, and 10 mg/day CLA significantly increased the concentration of mucin2 and goblet cells, but neither 5 mg/day CLA nor 2.5 mg/day CLA had any effects. Meanwhile, 40 and 20 mg/day CLA treatments significantly upregulated the concentration of tight junction proteins (ZO-1, occludin, and claudin-3) and ameliorated epithelial apoptosis caused by DSS. Moreover, oxidative-stress-related enzymes (superoxide dismutase, glutathione peroxidase, and catalase) and inflammatory cytokines [tumor necrosis factor-α, interleukin (IL)-10, and IL-6] were modulated by 40 and 20 mg/day CLA. Furthermore, 40 mg/day CLA rebalanced the gut microbiota damaged by DSS, including reducing Bacteroides and increasing Bifidobacterium and Odoribacter. In conclusion, CLA supplementation alleviated DSS-induced colitis in a dose-dependent manner by modulating inflammatory cytokines and oxidation stress, maintaining the mucosal barrier, and reverting microbiota changes.


Assuntos
Colite/tratamento farmacológico , Citocinas/metabolismo , Microbioma Gastrointestinal/efeitos dos fármacos , Ácidos Linoleicos Conjugados/administração & dosagem , Estresse Oxidativo/efeitos dos fármacos , Animais , Bactérias/classificação , Bactérias/efeitos dos fármacos , Bactérias/genética , Bactérias/isolamento & purificação , Colite/induzido quimicamente , Colite/metabolismo , Colite/microbiologia , Citocinas/genética , Sulfato de Dextrana/efeitos adversos , Humanos , Mucosa Intestinal/efeitos dos fármacos , Mucosa Intestinal/metabolismo , Mucosa Intestinal/microbiologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL
3.
J Agric Food Chem ; 67(41): 11408-11419, 2019 Oct 16.
Artigo em Inglês | MEDLINE | ID: mdl-31556290

RESUMO

In this study, the effects of 2-O-ß-d-glucopyranosyl-l-ascorbic acid (AA-2ßG), a natural ascorbic acid derivative from the fruits of Lycium barbarum, on treating the dextran sulfate sodium (DSS)-induced colitis in mice were investigated. The results revealed that AA-2ßG had palliating effects on DSS-induced inflammatory bowel disease (IBD) in terms of slowing down the trends of body weight and solid fecal mass loss, reducing colitis disease activity index, improving serum physiological and biochemical indicators, increasing colon length, blocking proinflammatory cytokines, and increasing tight junction proteins. Additionally, AA-2ßG treatment could promote the production of short-chain fatty acids and modulate the composition of the gut microbiota. The key bacteria related to IBD were found to be Porphyromonadaceae, Prevotellaceae, Rikenellaceae, Parasutterella, Parabacteroides, and Clostridium. The results indicated that AA-2ßG might treat IBD through the regulation of gut microbiota, suggesting that AA-2ßG has the potential to be used as a dietary supplement in the treatment of IBD.


Assuntos
Ácido Ascórbico/administração & dosagem , Colite/tratamento farmacológico , Microbioma Gastrointestinal/efeitos dos fármacos , Lycium/química , Extratos Vegetais/administração & dosagem , Animais , Ácido Ascórbico/química , Bactérias/classificação , Bactérias/efeitos dos fármacos , Bactérias/genética , Bactérias/isolamento & purificação , Colite/genética , Colite/imunologia , Colite/microbiologia , Citocinas/genética , Citocinas/imunologia , Sulfato de Dextrana/efeitos adversos , Modelos Animais de Doenças , Frutas/química , Humanos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Extratos Vegetais/química , Extratos Vegetais/isolamento & purificação
4.
J Agric Food Chem ; 67(34): 9522-9531, 2019 Aug 28.
Artigo em Inglês | MEDLINE | ID: mdl-31379161

RESUMO

The imbalance of T lymphocyte subsets substantially conduces to disturbed intestinal immune system and succeeding colonic tissue damage in inflammatory bowel diseases. It is considered that regulation of phytochemicals on cytokine production potentially provides a broad prospect for the exploitation of immunomodulatory agents. Here, we reported that oral administration of feruloylated oligosaccharides (FOs) effectively alleviated mice colitis disease induced by dextran sulfate sodium (DSS). FOs decreased the percentage of T helper (Th)17 cells and downregulated the production of Th17-specific cytokines. In contrast, FOs increased the percentage of regulatory T (Treg) cells and elevated the production of Treg-specific cytokines in colons of DSS-challenged mice. These results indicated that FOs restored the immunologic equilibrium of Th17 and Treg subsets, hereby ameliorating the deterioration of colitis. Furthermore, FOs diminished the secretion of interleukin (IL)-23 and IL-6 but enhanced the transforming growth factor-ß1 (TGF-ß1) in dendritic cells in vitro and in vivo, which contributed to the restoration of Th17 and Treg cells immune balance. The mechanistic analysis showed that the regulation of FOs on IL-23 and IL-6 was associated with the nuclear factor-κ-gene binding signaling pathway and TGF-ß1 with mitogen-activated protein kinase-activator protein 1 signaling pathway. Taken together, oral administration of FOs exerted potent immunomodulatory effects against mice colitis via restoring the immune balance of Th17 and Treg cells.


Assuntos
Colite/tratamento farmacológico , Oligossacarídeos/administração & dosagem , Animais , Colite/induzido quimicamente , Colite/genética , Colite/imunologia , Citocinas/genética , Citocinas/imunologia , Sulfato de Dextrana/efeitos adversos , Modelos Animais de Doenças , Humanos , Interleucina-23/genética , Interleucina-23/imunologia , Interleucina-6/genética , Interleucina-6/imunologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Oligossacarídeos/química , Transdução de Sinais/efeitos dos fármacos , Linfócitos T Reguladores/imunologia , Células Th17/imunologia
5.
Molecules ; 24(15)2019 Aug 03.
Artigo em Inglês | MEDLINE | ID: mdl-31382637

RESUMO

Backgrounds: This study aimed to investigate the protective effects of MMI-0100, a cell-penetrating peptide inhibitor of MAPK-activated protein kinase II (MK2), on acute colitis induced by dextran sodium sulfate (DSS). Mice were injected intraperitoneally with different doses of MMI-0100 (0.5 and 1 mg/kg per day, six days). The physiological indexes, the parameters for colonic pathological injury and the intensity of inflammatory responses were evaluated by histological staining, quantitative PCR, western blotting, and immunostaining. MMI-0100 attenuated DSS-induced body weight loss, colon length shortening, and colonic pathological injury, including decreased myeloperoxidase (MPO) and inhibited inflammatory cell infiltration. MMI-0100 suppressed DSS-induced activation of CD11b+ and F4/80 positive cell, and dramatically decreased the expression of a series of pro-inflammatory cytokines such as TNF-α, IL-6, IL-1ß, TGF- ß, IFN-γ, IL-17A, COX-2 and iNOS. A TUNEL assay showed that MMI-0100 protected against DSS-induced apoptosis. This is consistent with the results of Western blotting assay in apoptosis-related proteins including Bcl-2, BAX, caspase-3. The anti-inflammatory effects of MMI-0100 on DSS-induced colitis were achieved by down-regulating the phosphorylation level of MK2, IκBα and p65 protein. The current study clearly demonstrates a protective role for MMI-0100 in experimental IBD.


Assuntos
Anti-Inflamatórios/farmacologia , Peptídeos e Proteínas de Sinalização Intracelular/metabolismo , Peptídeos/farmacologia , Inibidores de Proteínas Quinases/farmacologia , Proteínas Serina-Treonina Quinases/metabolismo , Transdução de Sinais/efeitos dos fármacos , Animais , Apoptose/efeitos dos fármacos , Colite/tratamento farmacológico , Colite/etiologia , Colite/metabolismo , Citocinas/metabolismo , Sulfato de Dextrana/efeitos adversos , Mediadores da Inflamação/metabolismo , Camundongos , NF-kappa B/metabolismo , Fosforilação
6.
J Pharmacol Sci ; 140(2): 144-152, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-31242961

RESUMO

G protein-coupled receptor (GPR) 40 is a receptor for long-chain free fatty acids that enhances glucagon-like peptide (GLP)-2 production in intestinal L-cells. GLP-2 and its analogs have reported to increase remission rates in patients with Crohn's disease and improve experimental colitis in rodents. In the present study, we investigated the ameliorative effect of GPR40 activation in a dextran sulfate sodium (DSS)-induced murine colitis model using a specific GPR40 agonist, AS2034178. The daily administration of AS2034178 attenuated DSS-induced increases in the disease activity index, the shortening of the colon length, and the histological colonic injury, and increased the myeloperoxidase (MPO) activity and expression of inflammatory cytokines, in a dose-dependent manner. These effects were abolished by treatment with DC260126, a GPR40 antagonist, or GLP-2 (3-33), a GLP-2 antagonist. GPR40 was expressed in the colonic mucosa, which was colocalized with proglucagon, a precursor of GLP-2. AS2034178 significantly increased the amount of GLP-2 in the colonic tissue, which was abolished by DC260126 but not GLP-2 (3-33). Furthermore, AS2034178 significantly promoted the healing of DSS-induced colitis. These findings suggest that GPR40 activation ameliorates DSS-induced colitis in mice by enhancing GLP-2 production. Thus, GPR40 is a potential target for the treatment of IBD.


Assuntos
Compostos de Bifenilo/farmacologia , Compostos de Bifenilo/uso terapêutico , Colite/tratamento farmacológico , Colite/genética , Sulfato de Dextrana/efeitos adversos , Peptídeo 2 Semelhante ao Glucagon/metabolismo , Oxidiazóis/farmacologia , Oxidiazóis/uso terapêutico , Receptores Acoplados a Proteínas-G/agonistas , Receptores Acoplados a Proteínas-G/metabolismo , Regulação para Cima/genética , Animais , Compostos de Bifenilo/administração & dosagem , Colite/induzido quimicamente , Colite/metabolismo , Citocinas/metabolismo , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Células Enteroendócrinas/metabolismo , Mediadores da Inflamação/metabolismo , Masculino , Camundongos Endogâmicos C57BL , Terapia de Alvo Molecular , Oxidiazóis/administração & dosagem , Receptores Acoplados a Proteínas-G/fisiologia
7.
Food Funct ; 10(7): 3828-3838, 2019 Jul 17.
Artigo em Inglês | MEDLINE | ID: mdl-31187840

RESUMO

Honeys produced from medicinal plants hold great promise for human health. Herein, we determined the chemical composition and gastrointestinal protective effects of a novel monofloral honey from Prunella vulgaris (PVH). The physicochemical parameters (moisture, sugars, pH, protein content, diastase activity, and hydroxymethylfurfural) of the PVH samples met the criteria specified in European Union regulations and Chinese National Standards. Fifteen phenolic compounds were identified and quantified via high-performance liquid chromatography with a diode array detector and with time of flight tandem mass spectrometry detection (HPLC-DAD/Q-TOF-MS). Rosmarinic acid was found to be a potential marker for PVH identification. Using a dextran sulfate sodium (DSS)-induced acute colitis model, we demonstrated that the administration of PVH (5 g per kg b.w., p.o.) significantly decreased the disease activity index and mitigated colonic histopathological changes in rats. PVH also modulated the gut microbiota composition in the colitic rats, reversing the increase in the Bacteroidetes/Firmicutes ratio and restoring Lactobacillus spp. populations in DSS-challenged rats. The results of this study provide fundamental data on PVH, supporting its future application in the prevention of colitis.


Assuntos
Colite Ulcerativa/prevenção & controle , Sulfato de Dextrana/efeitos adversos , Microbioma Gastrointestinal/efeitos dos fármacos , Mel , Plantas Medicinais , Prunella/química , Animais , Bacteroidetes , Colite Ulcerativa/induzido quimicamente , Colo/metabolismo , Colo/patologia , Modelos Animais de Doenças , Firmicutes , Flores/química , Lactobacillus , Masculino , Ratos , Ratos Sprague-Dawley
8.
Eur J Pharmacol ; 857: 172453, 2019 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-31202807

RESUMO

Aesculin, a natural product from the traditional and widely-used Chinese medicine named Cortex fraxini, has attracted attention as a novel therapeutic modulator of inflammation. However, little is known about its effect on ulcerative colitis (UC). This study aimed to investigate the protective effects and mechanisms of aesculin on colitis. The results showed that, few cytotoxicity of aesculin were shown in vivo and in the RAW264.7 macrophages, while aesculin significantly relieved the symptoms of DSS-induced colitis and restrained the expression of inflammatory factors including iNOS, IL-1ß, TNF-α in both peritoneal macrophages and colonic tissues from DSS-induced mice and RAW264.7 macrophages. Of note, aesculin attenuated the activity of NF-κB signaling while promoted the nuclear localization of PPAR-γ in both rectal tissues from DSS-induced mice and LPS-stimulated macrophages. These findings demonstrated that the protection of aesculin against ulcerative colitis might be due to its regulation on the PPAR-γ and NF-κB pathway. Thus, aesculin could serve as a potential therapeutic agent for the treatment of ulcerative colitis.


Assuntos
Colite/metabolismo , Colite/prevenção & controle , Sulfato de Dextrana/efeitos adversos , Esculina/farmacologia , NF-kappa B/metabolismo , PPAR gama/metabolismo , Transdução de Sinais/efeitos dos fármacos , Animais , Colite/induzido quimicamente , Colite/patologia , Citocinas/biossíntese , Citoproteção/efeitos dos fármacos , Macrófagos/efeitos dos fármacos , Camundongos , Células RAW 264.7
9.
Food Funct ; 10(7): 4199-4209, 2019 Jul 17.
Artigo em Inglês | MEDLINE | ID: mdl-31250861

RESUMO

The anti-inflammatory profile of DPA was investigated via a dextran sulphate sodium (DSS)-induced colitis model, and was also compared with those of EPA and DHA. The results showed that DPA could significantly reduce (stronger than EPA and DHA) the disease activity index score, macroscopic appearance score, colon shortening, histological assessment, and myeloperoxidase accumulation in the colon. In addition, DPA also inhibited the abnormal production and mRNA expression of pro-inflammatory cytokines, namely tumor necrosis factor (TNF)-α, interleukin (IL)-1ß and IL-6 and improved the production and expression of an anti-inflammatory cytokine, IL-10. Furthermore, the molecular mechanisms underlying these effects were also explored through the synthesis pathway of eicosanoids. DPA could inhibit the synthesis of leukotriene B4 (LTB4) and prostaglandin E2 (PGE2) more greatly while differences of cyclooxygenase (COX) and 5-lipoxidase (LOX) contents in these three groups were not significant. We ascribed these effects to the easier incorporation of DPA into inflammatory cells leading to the decrease in the substrate for the synthesis of pro-inflammatory eicosanoids (PGE2 and LTB4). Besides, DPA-derived mediators might also be involved.


Assuntos
Anti-Inflamatórios/farmacologia , Colite Ulcerativa/tratamento farmacológico , Ácidos Graxos Insaturados/farmacologia , Inflamação/tratamento farmacológico , Animais , Peso Corporal , Colite Ulcerativa/patologia , Colo/metabolismo , Colo/patologia , Citocinas/metabolismo , Sulfato de Dextrana/efeitos adversos , Dinoprostona/metabolismo , Modelos Animais de Doenças , Ácidos Graxos Insaturados/isolamento & purificação , Interleucina-1beta , Leucotrieno B4/metabolismo , Lipoxigenase/metabolismo , Masculino , Camundongos , Extratos Vegetais/farmacologia , Prostaglandina-Endoperóxido Sintases/metabolismo , RNA Mensageiro/metabolismo , Fator de Necrose Tumoral alfa/metabolismo
10.
Food Funct ; 10(7): 3977-3991, 2019 Jul 17.
Artigo em Inglês | MEDLINE | ID: mdl-31204754

RESUMO

The fruit of Akebia trifoliata is popular in Asia, but researches concerning the phytochemicals of A. trifoliate pericarp extract (APE) and their metabolites, bioavailability, metabolism and anti-inflammatory activity in vivo are less known. In the present study, the chemical constituents of APE and their metabolites of rats after oral administration were identified using UPLC-LTQ-Orbitrap-MS/MS. A total of 18 compounds were tentatively characterized in APE, while 8 original compounds and 8 metabolites were observed in plasma, and 10 original compounds and 39 metabolites were detected in urine. Deglycosylation, glucuronidation, methylation and sulfation were the reactions that mainly occurred in the metabolism in vivo. Meanwhile, APE supplementation decreased dextran sulphate sodium (DSS)-induced colitis in mice, ameliorating epithelial barrier disruption, suppressing the proliferation and infiltration of immune cells, modulating the secretion of nitric oxide (NO) and prostaglandin E2 (PGE2), decreasing the expression of nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) as well as regulating oxidative stress in vivo. The results suggested that APE triterpenoids and their metabolites as major contributors to anti-inflammatory activities, providing a scientific basis for the use of APE as a functional food to ameliorate colon health in humans.


Assuntos
Anti-Inflamatórios/farmacologia , Colite/tratamento farmacológico , Sulfato de Dextrana/efeitos adversos , Metaboloma , Extratos Vegetais/farmacologia , Ranunculales/química , Animais , Disponibilidade Biológica , Colite/induzido quimicamente , Colo/patologia , Ciclo-Oxigenase 2/metabolismo , Dinoprostona/metabolismo , Modelos Animais de Doenças , Frutas/química , Masculino , Camundongos , Óxido Nítrico/metabolismo , Óxido Nítrico Sintase Tipo II/metabolismo , Compostos Fitoquímicos/farmacologia , Ratos , Espectrometria de Massas em Tandem
11.
Food Funct ; 10(7): 4046-4061, 2019 Jul 17.
Artigo em Inglês | MEDLINE | ID: mdl-31225554

RESUMO

Gallic acid (GA), a plant phenol found in fruits and vegetables, has been recently reported to attenuate ulcerative colitis (UC). However, the mechanism of GA in UC remains unknown. In this study, we investigated the therapeutic effects of GA on UC from the perspective of gut microbiota and supervised the metabolic alterations in vivo with 1H NMR-based metabolomics, which can provide a holistic view to understand the functions of GA in UC. Rats with dextra sulfate sodium (DSS)-induced colitis were rectally administrated with GA (6 mg kg-1) for 8 consecutive days. 16S gene sequencing was performed on feces samples to obtain bacterial community information. Urine and feces samples were analyzed with 1H NMR spectroscopy, and short chain fatty acids (SCFAs) in feces and colon contents were detected with gas chromatography. Our results showed that UC syndromes in the GA group were significantly attenuated. The microbial alterations in the DSS group were characterized by a decrease of probiotic bacteria, such as Lactobacillaceae and Prevotellaceae, and an increase of some pathogenic species, mainly in the Firmicutes and Proteobacteria phyla. GA treatment could modulate the microbiota composition towards a similar proportion to the control group. Metabolic data further revealed that the GA-induced metabolic changes focus on increasing carbohydrate metabolism (gluco-related metabolism) and bile acid (BA) metabolism and decreasing amino acid metabolism, which also provides evidence for alteration of the microbiota because these feces metabolites are by-products of interactions between the host and the microbiota. These findings demonstrate GA-induced alterations in metabolic and bacterial profiles in DSS-colitis, providing new insight into the attenuation of GA in UC.


Assuntos
Colite Ulcerativa/tratamento farmacológico , Ácido Gálico/farmacologia , Microbioma Gastrointestinal/efeitos dos fármacos , Metabolômica , Aminoácidos/metabolismo , Animais , Bactérias/classificação , Bactérias/genética , Colite Ulcerativa/induzido quimicamente , Colite Ulcerativa/patologia , Sulfato de Dextrana/efeitos adversos , Modelos Animais de Doenças , Ácidos Graxos Voláteis/análise , Fezes/química , Microbioma Gastrointestinal/genética , Metabolismo dos Lipídeos/efeitos dos fármacos , Espectroscopia de Ressonância Magnética , Masculino , Probióticos , RNA Ribossômico 16S/genética , Ratos , Ratos Sprague-Dawley , Urina/química
12.
Biosci Biotechnol Biochem ; 83(7): 1343-1353, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31038020

RESUMO

We previously reported that the major component of Enterococcus faecalis strain EC-12 (EC-12) inducing production of Interleukin (IL)-12 in mouse/human immune cells was its own RNA. This study aimed to investigate if RNase A-treated EC-12 could also produce IL-10 and to evaluate the possible effects of IL-10 produced by RNase A-treated EC-12. Three experiments were conducted: (1) Assessment of the effect of RNase A-treated EC-12 on transcriptome profiles and biological pathways in human peripheral blood mononuclear cells; (2) Determination of cytokine concentration in its culture supernatants; and (3) Supplementation of RNase A-treated EC-12 (RN) to mice with dextran sodium sulfate-induced colitis. Treatment of EC-12 with RNase A inhibited inflammatory response including the potency to induce IL-12 production, while it did not affect IL-10 production (Experiment 1 and 2). Colitis symptoms were milder in RN than in PBS-supplemented controls (Experiment 3). RNase A-treated EC-12 likely became an anti-inflammatory agent primarily inducing IL-10 production.


Assuntos
Anti-Inflamatórios/farmacologia , Enterococcus faecalis/efeitos dos fármacos , Ribonuclease Pancreático/farmacologia , Animais , Meios de Cultura , Sulfato de Dextrana/efeitos adversos , Humanos , Interleucina-10/biossíntese , Camundongos
13.
J Microbiol Biotechnol ; 29(4): 665, 2019 04 28.
Artigo em Inglês | MEDLINE | ID: mdl-31048595

RESUMO

This erratum is being published to correct the author's contribution of above manuscript by Chae et al. that was published in Journal of Microbiology and Biotechnology (2018, 28:11, 1800-1805). The ninth author (Jin Hyup Lee) should be marked as corresponding author (*) with latest author (Young Jun Kim). The correspondence should appear as: *Corresponding authors Young Jun Kim Phone: +82-44-860-1435; Fax: +82-44-860-1586; E-mail: yk46@korea.ac.kr Jin Hyup Lee Phone: +82-44-860-1437 Fax: +82-44-860-1586; E-mail: jinhyuplee@korea.ac.kr.


Assuntos
Bifidobacterium animalis/fisiologia , Colite/dietoterapia , Sulfato de Dextrana/efeitos adversos , Probióticos/uso terapêutico , Animais , Camundongos
14.
J Med Food ; 22(8): 851-860, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31074673

RESUMO

Aberrant crypt foci (ACF) is the precursor lesion of colorectal carcinogenesis (CRC), one of the most common malignancies in the world. Many studies have reported that people with higher phytochemical intake are at a reduced risk of developing ACF. One example of the botanical potential of preventive plant products is Cnidoscolus aconitifolius (CA), commonly known as Chaya. This study evaluated the phenolic profile of CA and the effects of the daily consumption of CA leaf infusion on the formation of ACF, histopathological lesions, and molecular biomarkers after azoxymethane (AOM) and dextran sulfate sodium (DSS) induced premalignant colon lesions in rats treated with for 16 and 32 weeks. The phenolic composition of the CA infusion was identified by reversed phase-high performance liquid chromatography-diode array detection (RP-HPCC-DAD). After sacrifice, a 4 cm segment was collected from the distal part of the colon and stained with methylene blue to look for ACF. Furthermore, 4 µm of colon, liver, and kidney was collected and stained with hematoxylin and eosin for histopathological analysis, along with 7 µm of colon for immunohistochemistry analysis. Eleven phenolic compounds were identified in the infusions, and ACF formation was reduced by 29.5% at the subchronic and by 64.6% at chronic stages. Lesions on kidney, liver, and colon tissue were also reduced. Our data suggest that CA treatment has preventive effects against AOM-/DSS-induced premalignant colon lesions in colon rats at the promotion level, inhibiting the cell proliferation of early neoplastic lesions and colonic inflammation through the decrease of ß-catenin by 41.8% at the subchronic stage and 29% at the chronic stage, along with a 46.2% reduction of cyclooxygenase 2 (COX-2) at long term, despite a high expression of NF-κB (30.3% at the subchronic stage and 22.8% at the chronic stage).


Assuntos
Focos de Criptas Aberrantes/prevenção & controle , Euphorbiaceae/química , Extratos Vegetais/administração & dosagem , Substâncias Protetoras/administração & dosagem , Focos de Criptas Aberrantes/induzido quimicamente , Focos de Criptas Aberrantes/patologia , Animais , Azoximetano/efeitos adversos , Colo/efeitos dos fármacos , Colo/patologia , Sulfato de Dextrana/efeitos adversos , Modelos Animais de Doenças , Humanos , Masculino , Extratos Vegetais/química , Folhas de Planta/química , Substâncias Protetoras/química , Ratos , Ratos Sprague-Dawley
15.
Eur J Pharmacol ; 855: 192-201, 2019 Jul 15.
Artigo em Inglês | MEDLINE | ID: mdl-31075241

RESUMO

Inflammatory bowel disease is an umbrella-term used to describe a set of chronic inflammatory conditions that affect the gastro-intestinal tract. Since most of the inflammatory medications in current use have several undesirable side-effects, stevioside, a naturally occurring, high-intensity sweetener was assessed in our study for its anti-inflammatory properties by in-vitro and in-vivo experiments. Stevioside was observed to significantly inhibit the levels of LPS induced elevation of cytokines, TNF-α (P < 0.05) and IL-6 (P < 0.001) as well as the production of reactive oxygen species (P < 0.01) and nitrites (P < 0.001) in RAW264.7 cells. Stevioside has also been evaluated for its anti-inflammatory effect by using dextran sulfate sodium (DSS)-induced ulcerative colitis model in mice. Stevioside significantly reduced the disease activity index (DAI) score, ameliorated the inflammatory symptoms induced by DSS in mice and exhibited intact colon histo-architecture. Stevioside treatment significantly inhibited the levels of pro-inflammatory cytokines, TNF-α and IL-6, and the protein expressions of pro-inflammatory mediators, COX-2 (P < 0.01) and iNOS (P < 0.01) and restored the levels of endogenous anti-oxidants such as superoxide dismutase (P < 0.01), catalase (P < 0.001), glutathione s-transferase (P < 0.001) and reduced glutathione (P < 0.001) level in colon tissues. It was also observed that stevioside significantly suppressed NF-κB (p65) activation by abrogating IκB phosphorylation and attenuated the phosphorylation of p38, ERK and JNK proteins in colon tissues. The findings of the present study suggest that stevioside exhibits anti-inflammatory property by inhibiting NF-κB (p65) and MAPK pathways and can be employed as an adjunct in nutraceuticals to treat IBD.


Assuntos
Anti-Inflamatórios/farmacologia , Colite Ulcerativa/induzido quimicamente , Colite Ulcerativa/tratamento farmacológico , Sulfato de Dextrana/efeitos adversos , Diterpenos de Caurano/farmacologia , Glucosídeos/farmacologia , Animais , Anti-Inflamatórios/uso terapêutico , Antioxidantes/metabolismo , Sobrevivência Celular/efeitos dos fármacos , Colite Ulcerativa/metabolismo , Colite Ulcerativa/patologia , Colo/efeitos dos fármacos , Colo/patologia , Citocinas/metabolismo , Diterpenos de Caurano/uso terapêutico , Glucosídeos/uso terapêutico , Mediadores da Inflamação/metabolismo , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , NF-kappa B/metabolismo , Nitritos/metabolismo , Estresse Nitrosativo/efeitos dos fármacos , Tamanho do Órgão/efeitos dos fármacos , Células RAW 264.7 , Espécies Reativas de Oxigênio/metabolismo
16.
J Med Food ; 22(7): 672-679, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31112045

RESUMO

Dietary products may protect against inflammatory bowel disease (IBD) through mechanisms such as forming gut microbiota structures and providing substrates for microbial metabolism. Recently, many studies have been conducted on diets that potentially alleviate or suppress IBD development. To assess the efficacy of dietary oils in treating IBD, we examined the protective effects of olive oil, coconut oil, corn oil, and cottonseed oil in a dextran sodium sulfate (DSS)-induced colitis mouse model. Treatment with cottonseed oil or corn oil ameliorated the severity of DSS-induced colitis, alleviating weight loss and preventing the shortening of the intestine. Moreover, cottonseed oil or corn oil treatment significantly reduced the expression of inflammatory cytokines such as tumor necrosis factor-α, interleukin (IL)-1ß, IL-6, and IL-17, as well as the expression of oxidative stress markers, including 8-hydroxyguanosine and nitrotyrosine in colon sections, compared with vehicle treatment. Cottonseed oil treatment inhibited intestinal fibrosis by reducing the expression of α-smooth muscle actin and type I collagen, compared with vehicle treatment in mice with DSS-induced colitis. Cottonseed oil protects against intestinal inflammation and the development of intestinal fibrosis by reducing inflammatory cytokines and oxidative stress markers, and may therefore be useful as a dietary product with therapeutic benefits for IBD.


Assuntos
Colite/prevenção & controle , Óleo de Sementes de Algodão/administração & dosagem , Substâncias Protetoras/administração & dosagem , Actinas/genética , Actinas/imunologia , Animais , Colite/induzido quimicamente , Colite/genética , Colite/imunologia , Colágeno Tipo I/genética , Colágeno Tipo I/imunologia , Sulfato de Dextrana/efeitos adversos , Modelos Animais de Doenças , Humanos , Interleucina-1beta/genética , Interleucina-1beta/imunologia , Interleucina-6/genética , Interleucina-6/imunologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Sulfatos/efeitos adversos , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/imunologia
17.
Drug Dev Res ; 80(5): 546-555, 2019 08.
Artigo em Inglês | MEDLINE | ID: mdl-30972795

RESUMO

The objective of the present work was to evaluate the anti-inflammatory effects of Vicenin-2 on dextran sulfate sodium (DSS)-induced colitis model. Colitis was induced in C57BL/6J mice by administration of 2% DSS in drinking water for 7 days. In addition to DSS, Vicenin-2 (50 mg kg-1 /day-1 ) was administrated orally to the test group. The ulceration extent and severity were assessed macroscopically, histopathologically, and by disease activity index. The Vicenin-2 treated group showed significant differences in physiological parameters including bodyweight, colon weight, and colon length, compared to DSS-induced colitis group. In addition, Vicenin-2 treatment effectively reduced stool consistency and bleeding scores. Myeloperoxidase (MPO) activity, expressions of pro-inflammatory cytokines, and specific key inflammatory markers (iNOS and COX-2) significantly increased in DSS-induced colitis colon tissues. However, administration of Vicenin-2 effectively reduced the MPO activity, attenuated the expression of pro-inflammatory cytokines and key inflammatory markers, in DSS-induced colitis mice. These results were comparable with sulfasalazine, an anti-inflammatory drug used routinely for ulcerative colitis (UC). These findings suggest that Vicenin-2 effectively suppresses DSS-induced colitis by attenuating expressions of key inflammatory mediators and found to be an attractive therapeutic drug for treating UC.


Assuntos
Anti-Inflamatórios não Esteroides/administração & dosagem , Apigenina/administração & dosagem , Colite/tratamento farmacológico , Ciclo-Oxigenase 2/metabolismo , Glucosídeos/administração & dosagem , Óxido Nítrico Sintase Tipo II/metabolismo , Administração Oral , Animais , Anti-Inflamatórios não Esteroides/farmacologia , Apigenina/farmacologia , Peso Corporal/efeitos dos fármacos , Colite/induzido quimicamente , Colite/metabolismo , Sulfato de Dextrana/efeitos adversos , Modelos Animais de Doenças , Regulação da Expressão Gênica/efeitos dos fármacos , Glucosídeos/farmacologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Tamanho do Órgão/efeitos dos fármacos , Peroxidase/metabolismo , Sulfassalazina/administração & dosagem , Sulfassalazina/farmacologia
18.
Food Funct ; 10(4): 1928-1939, 2019 Apr 17.
Artigo em Inglês | MEDLINE | ID: mdl-30869676

RESUMO

Glucomannans (GMs) from diverse natural plants have great potentiality in enhancing the host immune system. The protective effects of three GMs on the intestinal mucosal immunity in colitis mice were investigated and compared in this study. The three GMs (KGM, AGP, and DOP) were obtained from Amorphophallus rivieri, Aloe vera, and Dendrobium officinale, respectively, having different weight-averaged molecular weights (Mw), acetyl group content, and molar ratios of mannose to glucose (M/G). The three fractions were administered with or without dextran sodium sulfate (DSS) containing drinking water. Macroscopic observations (health state, crypt depth, and bowel thickness of colon tissue) were conducted. Furthermore, related cytokines and mRNA expressions of TLRs were measured by ELISA and RT-qPCR, respectively. Results showed that the administration of the three GMs improved the health state of colitis mice, such as the recovery of body weight, and the increase of the immune organ index, crypt depth, bowel wall thickness, and total number of immune cells. The integrity of intestinal mucosa was maintained by the increased number of goblet cells and mucin protein production. Further studies showed that GMs kept the balance between pro- and anti-inflammatory cytokines and also regulated the expressions of TLR-2, TLR-4, TLR-6, and TLR-9. The above results suggested that GMs could attenuate the intestinal epithelial injury and regulate the intestinal mucosal immunity. Structural features including the M/G ratio, Mw, and the content of acetyl groups jointly influence the protective effects of GMs on the colitis mice.


Assuntos
Aloe/química , Amorphophallus/química , Colite/prevenção & controle , Dendrobium/química , Mananas/administração & dosagem , Extratos Vegetais/administração & dosagem , Substâncias Protetoras/administração & dosagem , Animais , Colite/induzido quimicamente , Colite/genética , Colite/imunologia , Citocinas/genética , Citocinas/imunologia , Sulfato de Dextrana/efeitos adversos , Feminino , Humanos , Mucosa Intestinal/efeitos dos fármacos , Mucosa Intestinal/imunologia , Camundongos , Camundongos Endogâmicos BALB C , Receptor 2 Toll-Like/genética , Receptor 2 Toll-Like/imunologia , Receptor 4 Toll-Like/genética , Receptor 4 Toll-Like/imunologia , Receptor 6 Toll-Like/genética , Receptor 6 Toll-Like/imunologia
19.
Int J Mol Sci ; 20(6)2019 Mar 22.
Artigo em Inglês | MEDLINE | ID: mdl-30909435

RESUMO

Renal disease is not rare among patients with inflammatory bowel disease (IBD) and is gaining interest as a target of research. However, related changes in glomerular structural have rarely been investigated. This study was aimed at clarifying the changes in collagens and glomerular filtration barrier (GFB)-related proteins of glomeruli in a dextran sulfate sodium (DSS)-induced colitis mouse model. Acute colitis was induced by administering 3.5% DSS in Slc:ICR strain mice for eight days. Histological changes to glomeruli were examined by periodic acid-Schiff (PAS) and Masson's trichrome staining. Expressions of glomerular collagens and GFB-related proteins were analyzed by immunofluorescent staining and Western blot analysis. DSS-colitis mice showed an elevated disease activity index (DAI), colon shortening, massive cellular infiltration and colon damage, confirming that DSS-colitis mice can be used as an IBD animal model. DSS-colitis mice showed increased glycoprotein and collagen deposition in glomeruli. Interestingly, we observed significant changes in glomerular collagens, including a decrease in type IV collagen, and an increment in type I and type V collagens. Moreover, declined GFB-related proteins expressions were detected, including synaptopodin, podocalyxin, nephrin and VE-cadherin. These results suggest that renal disease in DSS-colitis mice might be associated with changes in glomerular collagens and GFB-related proteins. These findings are important for further elucidation of the clinical pathological mechanisms underlying IBD-associated renal disease.


Assuntos
Colite/etiologia , Colite/metabolismo , Colágeno/metabolismo , Barreira de Filtração Glomerular/metabolismo , Glomérulos Renais/metabolismo , Animais , Biomarcadores , Biópsia , Colite/patologia , Sulfato de Dextrana/efeitos adversos , Modelos Animais de Doenças , Progressão da Doença , Imuno-Histoquímica , Camundongos , Modelos Biológicos
20.
Int J Mol Sci ; 20(6)2019 Mar 23.
Artigo em Inglês | MEDLINE | ID: mdl-30909599

RESUMO

Intravenous immunoglobulin (IVIg) therapy has diverse anti-inflammatory and immunomodulatory effects and has been employed successfully in autoimmune and inflammatory diseases. The role of IVIg therapy in the modulation of intestinal inflammation and fungal elimination has not been yet investigated. We studied IVIg therapy in a murine model of dextran sulfate sodium (DSS)-induced colitis. Mice received a single oral inoculum of Candida albicans and were exposed to DSS treatment for 2 weeks to induce colitis. All mice received daily IVIg therapy starting on day 1 for 7 days. IVIg therapy not only prevented a loss of body weight caused by the development of colitis but also reduced the severity of intestinal inflammation, as determined by clinical and histological scores. IVIg treatment significantly reduced the Escherichia coli, Enterococcus faecalis, and C. albicans populations in mice. The beneficial effects of IVIg were associated with the suppression of inflammatory cytokine interleukin (IL)-6 and enhancement of IL-10 in the gut. IVIg therapy also led to an increased expression of peroxisome proliferator-activated receptor gamma (PPARγ), while toll-like receptor 4 (TLR-4) expression was reduced. IVIg treatment reduces intestinal inflammation in mice and eliminates C. albicans overgrowth from the gut in association with down-regulation of pro-inflammatory mediators combined with up-regulation of anti-inflammatory cytokines.


Assuntos
Candida albicans/imunologia , Colite/tratamento farmacológico , Colite/etiologia , Homeostase/efeitos dos fármacos , Homeostase/imunologia , Imunoglobulinas Intravenosas/administração & dosagem , Intestinos/imunologia , Intestinos/microbiologia , Animais , Carga Bacteriana , Colite/diagnóstico , Colite/mortalidade , Contagem de Colônia Microbiana , Citocinas/metabolismo , Sulfato de Dextrana/efeitos adversos , Modelos Animais de Doenças , Imuno-Histoquímica , Mediadores da Inflamação , Camundongos , Índice de Gravidade de Doença , Resultado do Tratamento
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