• Korean Journal of Medicinal Crop Science
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• v.19 no.1
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• pp.16-23
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• 2011

This study was conducted to investigate the anti-inflammatory effects of Pruns mume, Schisandra chinensis, Chaenomeles sinensis-- Prunus mume mixtrue (PM) treatment on colitis induced in mice by dextran sodium sulfate (DSS) treatment. A total of 25 male BALB/c mice (average weight $20.7\;{\pm}\; 1.6 \;g$) were divided into 5 treatment groups and fed a commercial diet (A), PM administration (B), commercial diet + induced colitis by DSS (C), PM administration + induced colitis by DSS (D) and sulfasalazine + induced colitis by DSS (E). We found that PM treatment (D) and sulfasalazine (E) decreased the expression of $TNF-{\alpha}$ and COX-2 compared to the DSS-induced colitis group (C). The expression of IL-4, STAT6, $IFN-{\gamma}$, STAT1 was decreased in group D and group E compared to the colitis group (C), COX-2 and STAT1 were more decreased in group D. The serum IgE levels decreased in the PM treatment groups (C and D) compared to the non-PM treatment groups (A and B) although there was no significant difference between the PM treatment groups. It is notable that a therapeutic application of the PM extracts ameliorated DSS-induced colitis in mice.

• Herbal Formula Science
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• v.16 no.2
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• pp.171-182
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• 2008

The aqueous extract of Schisandra chinensis, Evodia rutaecarpa and meal (SEM-Ex) has been traditionally used in the Oriental countries as an astringent. However, little is known about the effects of aqueous extract of SEM-Ex on dextran-sulfate sodium (DSS)-induced colitis in mice. In this study, we investigated the protective effects of SEM-Ex on DSS-induced colitis in mice. An experimental colitis was induced by daily treatment with 5% DSS. SEM-Ex was orally administered from day 2 of DSS treatment in the different dose (10-50 mg/kg body weight). SEM-Ex reduced significantly clinical sign of DSS-induced colitis, including body weight loss, shorten colon length, increased disease activity index (DAI), and histological colon injury. Moreover, SEM-Ex suppressed significantly not only the serum haptoglobin levels and the activities of myeloperoxidase (MPO), but also the colon tissue expression levels of monocyte chemoattractant protein-1 (MCP-1) in DSS-induced mice. In contrast, SEM-Ex increased significantly the colon tissue expression levels of granular colony stimulating factor (G-CSF) well known as anti-inflammatory cytokine. These results suggest that SEM-Ex administration could reduce significantly the clinical signs and regulate of chemokine and anti-inflammatory cytokine in DSS-induced model mice. Therefore, these properties may contribute to the strong anti-ulcerative colitis (UC) response effect of SEM-Ex.

• Korean Journal of Pharmacognosy
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• v.39 no.2
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• pp.104-109
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• 2008

We previously reported that anti-inflammatory properties of poncirin, isolated from fruit of Poncirus trifoliata, might be the result from the inhibition of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis $factor-{\acute{a}}$ ($TNF-{\alpha}$) and interlukin-6 (IL-6) expression via the down-regulation of $NF{-\kappa}B$ binding activity. In this study, we investigated whether poncirin has an inhibitory effect on the production of pro-inflammatory mediators ex vivo and whether poncirin could relieve the symptoms of dextran sulfate sodium (DSS)-induced colitis in mice model of inflammatory bowel disease. Poncirin significantly inhibited the productions of NO, IL-6 and $TNF-{\alpha}$ in lipopolysaccharide (LPS)-induced mouse peritoneal macrophage. In addition, poncirin-treated mice when compared to control mice not receiving treatment recovered better from the weight loss caused by DSS-induced colitis. Changes in disease activity index (DAI) of poncirin-treated mice were also more favorable than for control mice and were comparable with mice treated with a typical anti-inflammatory-drug, 5-aminosalichylic acid (5-ASA). In addition, suppression of plasma NO and IL-6 productions of poncirin-treated mice was also observed in DSS-induced colitis. These results suggest that poncirin has potentially useful anti-inflammatory effects mediated by suppression of inflammatory mediator productions.

• Journal of Pharmaceutical Investigation
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• v.37 no.5
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• pp.269-273
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• 2007

Poorly water-soluble ibuprofen and ethanol can be encapsulated in gelatin microcapsule by spray drying technique. To select an optimal formula of ibuprofen-loaded gelatin microcapsule which increased the ethanol content and ibuprofen solubility with the decreased amount of gelatin in the microcapsules, in this study, the effect of gelatin, ibuprofen and sodium lauryl sulfate on the ibuprofen solubility and the amount of ethanol and ibuprofen encapsulated in the gelatin microcapsule were investigated. Ibuprofen solubility and the amount of ethanol encapsulated increased as gelatin and sodium lauryl sulfate increased, reached maximum at 4% and 0.6%, respectively and then followed a rapid decrease. Furthermore, the ibuprofen solubility and the encapsulated ibuprofen content increased as the amount of ibuprofen increased, reaching maximum at 0.5% and beyond that, there was no change in the solubility and ibuprofen content. However, the encapsulated ethanol content remained same irrespective of the amount of ibuprofen. On the basis of increased ibuprofen solubility, our results showed that the formula of ibuprofen-loaded gelatin microcapsule at the ratio of gelatin/ibuprofen/sodium lauryl sulfate/water/ethanol of 4/0.5/0.6/30/70 with ibuprofen solubility of about $290\;{\mu}g/mL$ and ethanol content of about $160\;{\mu}g/mg$ could be a potential oral delivery system for poorly water-soluble ibuprofen.

• Journal of Ginseng Research
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• v.39 no.1
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• pp.14-21
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• 2015

Background: Colorectal cancer is a leading cause of cancer-related death, and inflammatory bowel disease is a risk factor for this malignancy. We previously reported colon cancer chemoprevention potential using American ginseng (AG) in a xenograft mice model. However, the nude mouse model is not a gut-specific colon carcinogenesis animal model. Methods: In this study, an experimental colitis and colitis-associated colorectal carcinogenesis mouse model, chemically induced by azoxymethane/dextran sodium sulfate (DSS) was established and the effects of oral AG were evaluated. The contents of representative ginseng saponins in the extract were determined. Results: AG significantly reduced experimental colitis measured by the disease activity index scores. This suppression of the experimental colitis was not only evident during DSS treatment, but also very obvious after the cessation of DSS, suggesting that the ginseng significantly promoted recovery from the colitis. Consistent with the anti-inflammation data, we showed that ginseng very significantly attenuated azoxymethane/DSS-induced colon carcinogenesis by reducing the colon tumor number and tumor load. The ginseng also effectively suppressed DSS-induced proinflammatory cytokines activation using an enzyme-linked immunosorbent assay array, in which 12 proinflammatory cytokine levels were assessed, and this effect was supported subsequently by real-time polymerase chain reaction data. Conclusion: AG, as a candidate of botanical-based colon cancer chemoprevention, should be further investigated for its potential clinical utility.

• The Korean Journal of Food And Nutrition
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• v.34 no.2
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• pp.146-155
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• 2021

This study observed the anti-inflammatory effect of the polysaccharide derived from the mycelium of Tremella fuciformis in mice with colitis induced with dextran sulfate sodium (DSS). The experimental groups were normal, DSS, DSS-TFL50, DSS-TFH100, and suflasalazine. Body weights, colon lengths, and organ weights were measured, and the plasma level of pro-inflammatory cytokine and mRNA and protein expression in colon tissue were analyzed. Body weight loss, a symptom of DSS-induced colitis, was suppressed by DSS-TF and the speed of weight recovery proceeded rapidly. In addition, DSS-TF showed a significant inhibitory effect on the decrease of colon length typically caused by colon damage. TNF-α, IL-6 and IL-1β cytokine levels in plasma were reduced in DSS-TF and positive control groups. TNF-α, COX-2 and IL-1β mRNA expression in colon tissue were inhibited in DSS-TF and positive control, and it was significantly different from that of the DSS group. The protein expression of inflammation-related genes (IL-6, TNF-α and COX-2) in the colon tissue was significantly increased by DSS compared to that of the normal group, but by DSS-TFL50, DSS-TFH100 and sulfasalarin decreased. In conclusion, the polysaccharide derived from the mycelium of Tremella fuciformis showed the anti-inflammatory effect on DSS-induced colitis in mice.

• Clinical Psychopharmacology and Neuroscience
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• v.16 no.4
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• pp.422-433
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• 2018

Objective: Neuropsychiatric manifestations like depression and cognitive dysfunction commonly occur in inflammatory bowel disease (IBD). In the context of the brain-gut axis model, colitis can lead to alteration of brain function in a bottom-up manner. Here, the changes in the response of the hypothalamic-pituitary-adrenal axis and inflammation-related markers in the brain in colitis were studied. Methods: Dextran sodium sulfate (DSS) was used to generate a mouse model of colitis. Mice were treated with DSS for 3 or 7 days and sacrificed. We analyzed the gene expression of brain-derived neurotrophic factor (BDNF), cyclooxygenase 2 (COX-2), and glial fibrillary acidic protein (GFAP), and the expression of GFAP, in the hippocampus, hypothalamus, and amygdala. Additionally, the levels of C-reactive protein (CRP) and serum cortisol/corticosterone were measured. Results: Alteration of inflammatory-related markers varied depending on the brain region and exposure time. In the hippocampus, COX-2 mRNA, GFAP mRNA, and GFAP expression were upregulated during exposure to DSS. However, in the hypothalamus, COX-2 mRNA was upregulated only 3 days after treatment. In the amygdala, BDNF and COX-2 mRNAs were downregulated. CRP and corticosterone expression increased with DSS treatment at day 7. Conclusion: IBD could lead to neuroinflammation in a bottom-up manner, and this effect varied according to brain region. Stress-related hormones and serum inflammatory markers, such as CRP, were upregulated from the third day of DSS treatment. Therefore, early and active intervention is required to prevent psychological and behavioral changes caused by IBD, and region-specific studies can help understand the precise mechanisms by which IBD affects the brain.

• Korean Journal of Chemical Engineering
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• v.35 no.11
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• pp.2269-2282
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• 2018

Mixed micelle formation behavior of cationic surfactant-cetyltrimethylammonium bromide (CTAB) and anionic surfactant sodium dodecyl sulfate (SDS) in aqueous as well as in urea medium from 303.15 K to 323.15 K at 5 K interval was carried out by conductometric method. The differences between the experimental values of critical micelle concentrations (cmc) and ideal critical micelle concentrations ($cmc^{id}$) illustrate the interaction between the amphiphiles studied. The values of micellar mole fraction ($X_1^{Rub}$ (Rubingh), $X_1^M$ (Motomura), $X_1^{Rod}$ (Rodenas) and $X_1^{id}$(ideal) of surfactant CTAB determined by different proposed models and outcome indicate high involvement of CTAB in SDS-CTAB mixed micellization, which enhance by means of the augment of mole fraction of CTAB. The negative value of interaction parameter (${\beta}$) showed an attractive interaction involving CTAB and SDS. Activity coefficients were less than unity in all case, which also reveals the presence of interaction between CTAB & SDS. The negative ${\Delta}G^0_m$ values imply the spontaneous mixed micellization phenomenon. The attained values of ${\Delta}H^0_m$ were positive at inferior temperature, while negative at superior temperature. The negative ${\Delta}H^0_m$ values in urea ($NH_2CONH_2$) medium illustrate exothermic micellization process. The magnitudes of ${\Delta}S^0_m$ were positive in almost all cases. The excess free energy of mixed micelle formation (${\Delta}G_{ex}$) was found to be negative, which indicates the stability of mixed micelle as compared to the individual's components micelles.

• Parasites, Hosts and Diseases
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• v.60 no.5
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• pp.309-315
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• 2022

Inflammatory bowel disease (IBD) is a chronic and recurrent illness of the gastrointestinal tract. Treatment of IBD traditionally involves the use of aminosalicylic acid and steroids, while these drugs has been associated with untoward effects and refractoriness. The absence of effective treatment regimen against IBD has led to the exploration of new targets. Parasites are promising as an alternative therapy for IBD. Recent studies have highlighted the use of parasite-derived substances, such as excretory secretory products, extracellular vesicles (EVs), and exosomes, for the treatment of IBD. In this report, we examined whether EVs secreted by Giardia lamblia could prevent colitis in a mouse model. G. lamblia EVs (GlEVs) were prepared from in vitro cultures of Giardia trophozoites. Clinical signs, microscopic colon tissue inflammation, and cytokine expression levels were detected to assess the effect of GlEV treatment on dextran sulfate sodium (DSS)-induced experimental murine colitis. The administration of GlEVs prior to DSS challenge reduced the expression levels of pro-inflammatory cytokines, including tumor necrosis factor alpha, interleukin 1 beta, and interferon gamma. Our results indicate that GlEV can exert preventive effects and possess therapeutic properties against DSS-induced colitis.

• Biomolecules & Therapeutics
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• v.30 no.6
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• pp.510-519
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• 2022

Tofacitinib, a Janus kinase 1 and 3 inhibitor, is mainly metabolized by CYP3A1/2 and CYP2C11 in the liver. The drug has been approved for the chronic treatment of severe ulcerative colitis, a chronic inflammatory bowel disease. This study investigated the pharmacokinetics of tofacitinib in rats with dextran sulfate sodium (DSS)-induced ulcerative colitis. After 1-min of intravenous infusion of tofacitinib (10 mg/kg), the area under the plasma concentration-time curves from time zero to time infinity (AUC) of tofacitinib significantly increased by 92.3%. The time-averaged total body clearance decreased significantly by 47.7% in DSS rats compared with control rats. After the oral administration of tofacitinib (20 mg/kg), the AUC increased by 85.5% in DSS rats. These results could be due to decreased intrinsic clearance of the drug caused by the reduction of CYP3A1/2 and CYP2C11 in the liver and intestine of DSS rats. In conclusion, ulcerative colitis inhibited CYP3A1/2 and CYP2C11 in the liver and intestines of DSS rats and slowed the metabolism of tofacitinib, resulting in increased plasma concentrations of tofacitinib in DSS rats.