APicrorhiza kurroaDerivative, Picroliv, Attenuates the Development of Dextran-Sulfate-Sodium-Induced Colitis in Mice

Background. Free radicals and proinflammatory cytokines have been shown to play a critical role in the pathogenesis of ulcerative colitis (UC). Picroliv, aPicrorhiza kurroaderivative, has been demonstrated to have antioxidant and anti-inflammatory effect. The purpose of the study was to investigate the effects of picroliv on experimental model of UC in mice.Materials and Methods. Picroliv was administrated orally by gavage to mice with colitis induced by dextran sulfate sodium (DSS). Disease activity index (DAI), colon length, and histology score were observed. Myeloperoxidase (MPO) activity, and SOD, MDA concentrations were measured by enzyme-linked immunosorbent assay (ELISA) while the expression of cytokine mRNAs was studied by real-time-quantitative polymerase chain reaction and also ELISA. The expression of NF-κB p65 was observed by immunohistochemistry staining and western blotting.Results. A significant improvement was observed in DAI and histological score in mice treated with picroliv, and incerased MPO activity, MDA concentrations, and the expression of IL-1β, TNF-α, and NF-κB p65 in mice with DSS-induced colitis were significantly reduced while decreased SOD level increased following administration of picroliv.Conclusion. The administration of picroliv leads to an amelioration of DSS-induced colitis, suggesting administration of picroliv may provide a therapeutic approach for UC.

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The protective effect of curcumin on rats with DSS-induced ulcerative colitis and its mechanisms

10.21203/rs.3.rs-191627/v1 ◽

2021 ◽

Author(s):

Jing Guo ◽

Yan-yan Zhang ◽

Mei Sun ◽

Ling-fen Xu

Keyword(s):

Ulcerative Colitis ◽

Th17 Cells ◽

Dextran Sulfate ◽

Activity Index ◽

Disease Activity Index ◽

Treg Cells ◽

Enzyme Linked Immunosorbent Assay ◽

T Helper ◽

T Helper 17 ◽

Inflammatory Bowel

Abstract Aim This study aimed to explore effect of curcumin on inflammatory bowel disease (IBD) in rats and its mechanism.Methods: A dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) rat model was established. The disease activity index (DAI) scores were calculated. The histopathological damage scores were determined by haematoxylin-eosin (H&E) staining. Regulatory T (Treg) cells and T helper 17 (Th17) cells in the spleen were analysed by flow cytometry. The levels of interleukin (IL)-10 and IL-17A were determined by enzyme-linked immunosorbent assay (ELISA). Results: Compared with the DSS model group, the curcumin group exhibited significantly reduced DAI scores and improvements in histopathological damage. The expression of CD4+IL-17+ Th17 cells was significantly lower and the expression of CD4+CD25+Foxp3+ Treg cells was significantly higher in the curcumin group than in the DSS group.Conclusion: Curcumin may be a new and effective treatment for IBD by regulating the balance of Treg/Th17 cells and the expression of IL-10 and IL-17A.

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Suppression of Th17 Cell Response in the Alleviation of Dextran Sulfate Sodium-Induced Colitis by Ganoderma lucidum Polysaccharides

Journal of Immunology Research ◽

10.1155/2018/2906494 ◽

2018 ◽

Vol 2018 ◽

pp. 1-10 ◽

Cited By ~ 3

Author(s):

Bing Wei ◽

Ran Zhang ◽

Jingbo Zhai ◽

Junfeng Zhu ◽

Fangli Yang ◽

...

Keyword(s):

Weight Loss ◽

Body Weight ◽

Ganoderma Lucidum ◽

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Therapeutic Potential ◽

Activity Index ◽

Survival Rates ◽

Body Weight Loss ◽

Disease Activity Index

Background. Ganoderma lucidum polysaccharides (GLP) has anti-inflammatory and immunomodulatory effects. Dysregulated immune responses are involved in the pathogenesis of dextran sulfate sodium (DSS)-induced colitis. The aim of this study was to assess the therapeutic potential of GLP to alleviate DSS-induced colitis. Methods. The mice were administered with GLP by intragastric gavage daily for two weeks prior to the DSS treatment. Mice were orally administered with 2.5% DSS dissolved in drinking water with GLP or water treatment for 6 days. The mice were killed on day 7 after induction of colitis. Survival rates, body weight loss, colon lengths, histological changes, and disease activity index scores (DAI) were evaluated. Results. GLP significantly improved survival rates, colon length shortening, body weight loss, histopathological score, and DAI scores in mice with DSS-induced colitis. GLP markedly suppressed the secretions of TNF-α, IL-1β, IL-6, IL-17A, and IL-4 and significantly affected populations of Th17 cells, B cells, NK cells, and NKT cells in the lamina propria lymphocytes. Conclusions. GLP prevented inflammation, maintained intestinal homeostasis, and regulated the intestinal immunological barrier functions in mice with DSS-induced colitis.

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Suppression of Dextran Sulfate Sodium-Induced Colitis in Mice by Radon Inhalation

Mediators of Inflammation ◽

10.1155/2012/239617 ◽

2012 ◽

Vol 2012 ◽

pp. 1-11 ◽

Cited By ~ 33

Author(s):

Yuichi Nishiyama ◽

Takahiro Kataoka ◽

Keiko Yamato ◽

Takehito Taguchi ◽

Kiyonori Yamaoka

Keyword(s):

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Activity Index ◽

Disease Activity Index ◽

Myeloperoxidase Activity ◽

Protective Effects ◽

Necrosis Factor Alpha ◽

Activated Neutrophils ◽

Radon Inhalation ◽

Activity Index Score

The enhanced release of reactive oxygen species from activated neutrophils plays important role in the pathogenesis of inflammatory bowel disease. We previously reported that radon inhalation activates antioxidative functions in various organs of mice. In this study, we examined the protective effects of radon inhalation on dextran sulfate sodium- (DSS) induced colitis in mice which were subjected to DSS for 7 days. Mice were continuously treated with air only (sham) or radon at a concentration of 2000 Bq/m3from a day before DSS administration to the end of colitis induction. In the results, radon inhalation suppressed the elevation of the disease activity index score and histological damage score induced by DSS. Based on the changes in tumor necrosis factor-alpha in plasma and myeloperoxidase activity in the colon, it was shown that radon inhalation suppressed DSS-induced colonic inflammation. Moreover, radon inhalation suppressed lipid peroxidation of the colon induced by DSS. The antioxidant level (superoxide dismutase and total glutathione) in the colon after DSS administration was significantly higher in mice treated with radon than with the sham. These results suggested that radon inhalation suppressed DSS-induced colitis through the enhancement of antioxidative functions in the colon.

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The effect of selected Lactobacillus strains on dextran sulfate sodium-induced mouse colitis model

Acta Microbiologica et Immunologica Hungarica ◽

10.1556/030.2020.00834 ◽

2020 ◽

Author(s):

Meysam Hasannejad-Bibalan ◽

Ali Mojtahedi ◽

Morteza Eshaghi ◽

Mahdi Rohani ◽

Mohammad Reza Pourshafie ◽

...

Keyword(s):

Histological Analysis ◽

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Activity Index ◽

Lactobacillus Rhamnosus ◽

Disease Activity Index ◽

Therapeutic Effects ◽

Probiotic Properties ◽

Markers Of Inflammation ◽

Colitis Model

AbstractInflammatory bowel disease (IBD) comprises two major illnesses: Crohn's disease (CD) and ulcerative colitis (UC). Dextran sulfate sodium (DSS) mouse colitis model has been used in understanding the mechanism of IBD. This study was conducted to examine selected Lactobacillus spp. as potential IBD treatment in the DSS-induced animal model. Balb/c mice were used and colitis was induced by adding 5% dextran sodium sulfate into the drinking water for 8 days. Colon length, disease activity index (DAI) and histological analysis were measured as markers of inflammation in DSS colitis mice. The majority of the Lactobacillus species significantly prevented the shortening of the colon length compared with the DSS group. The DAI scores of mice were significantly reduced following usage of four Lactobacillus strains included: Lactobacillus plantarum 03 and 06, Lactobacillus brevis 02 and Lactobacillus rhamnosus 01. The histological analysis exhibited that oral administration of Lactobacillus strains had therapeutic effects on mice colitis. L. plantarum and L. brevis showed better therapeutic effect against DSS-induced acute colitis mice. The probiotic activities of these three isolates indicated that the probiotic effects were strain specific and none of these useful bacteria could exhibit all of the valued probiotic properties simultaneously.

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The Potential of Vitamin D3 to Repaired Mucosal Injury in Dextran Sulfate Sodium Induced Acute Colitis in Mice

Open Access Macedonian Journal of Medical Sciences ◽

10.3889/oamjms.2021.6700 ◽

2021 ◽

Vol 9 (B) ◽

pp. 931-936

Author(s):

Satrio Wibowo ◽

Krisni Subandiyah ◽

Kusworini Handono ◽

Sri Poeranto

Keyword(s):

Stem Cell ◽

Vitamin D3 ◽

Cell Activation ◽

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Activity Index ◽

Disease Activity Index ◽

Mucosal Injury ◽

Potential Effect ◽

Mucosal Repair

BACKGROUND: Inflammatory Bowel Disease (IBD) has become an emerging disease worldwide. The treatment of IBD involves two basic principles: Inflammation control and mucosal repair. AIM: This study evaluates the potential effect of Vitamin D3 in mucosal repair through colon stem cell activation and proliferation. METHODS: Dextran sulfate sodium (DSS; 5%) was used to induce colitis in mice. Vitamin D3 at various dosages was then administered as a treatment. The mice were divided into five groups: Control (C-); DSS only (C+); and DSS (5%) plus Vitamin D3 at 0.2 μg (VD1), 0.4 μg (VD2), or 0.6 μg (VD3) per 25 g body weight as the treatment groups. Immunofluorescence analyses of Lgr5+ expression indicated stem cell activation, and Ki67 expression indicated stem cell proliferation. The disease activity index (DAI), colon length, and histopathological index scores were determined after treatment to assess the inflammation and severity of colitis. RESULTS: Immunofluorescence analyses showed a gradually increasing expression of Lgr5+ also Ki67 in proportion with high doses group of Vitamin D3 (p < 0.05). The colon length, DAI scores, and histopathological index scores improved in all groups after Vitamin D3 treatment (p = 0.05; p = 0.026; and p = 0.029, respectively). CONCLUSION: Vitamin D3 has a potential beneficial effect on amplifying intestinal stem cells regulated by Wnt/B-catenin signaling. It is also reduced the inflammatory process proved by the evaluation severity of colitis. It might play an essential role in mucosal repair in IBD.

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Natural naphthoquinones isolated from Lithospermum erythrorhizon suppress dextran sulfate sodium-induced murine experimental colitis

10.1101/830224 ◽

2019 ◽

Author(s):

Wenxue Sun ◽

Hongwei Han ◽

Zhaoyue Wang ◽

Zhongling Wen ◽

Minkai Yang ◽

...

Keyword(s):

Nlrp3 Inflammasome ◽

Active Sites ◽

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Activity Index ◽

Docking Simulation ◽

Disease Activity Index ◽

Experimental Colitis ◽

Intragastric Administration ◽

Underlying Mechanisms

AbstractThe purpose of this study was to explore the effects of natural shikonin and its derivatives on mice experimental colitis induced by dextran sulfate sodium, and to investigate the underlying mechanisms in vivo. Our results suggested that, intragastric administration of single compound like shikonin and its derivatives contributed to attenuating symptoms of malignant induced by DSS. Meanwhile, shikonin or its derivatives could also remarkably reduce the disease activity index and histopathological scores, suppress the levels of pro-inflammatory cytokines (including IL-6, IL-1β and TNF-α), while increase that of inflammatory cytokine IL-10 in serum. Additionally, both shikonin and alkanin were found to restrain the levels of COX-2, MPO and iNOS in serum and colonic tissues. Moreover, western blotting results demonstrated that shikonin and its derivatives could inhibit the activation of the NLRP3 inflammasome and the NF-κB signaling pathway, relieve the DSS-induced disruption of colonic epithelial tight junction (TJ) in colonic tissues. Further, docking simulation had been performed to prove that shikonin and its derivatives could bind to the active sites of NLRP3 inflammasome and the NF-κB to generate an effective inflammatory effect. Taken together, our experimental data can provide some evidence for the potential use of shikonin and its derivatives to treat the inflammatory bowel disease (IBD).

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Clinical and Structural Effects of Traditional Chinese Medicine and the Herbal Preparation, Iberogast, in a Rat Model of Ulcerative Colitis

Journal of Evidence-Based Complementary & Alternative Medicine ◽

10.1177/2156587213503660 ◽

2013 ◽

Vol 19 (1) ◽

pp. 10-19 ◽

Cited By ~ 9

Author(s):

Suzanne Mashtoub ◽

Bang V. Hoang ◽

Megan Vu ◽

Kerry A. Lymn ◽

Christine Feinle-Bisset ◽

...

Keyword(s):

Ulcerative Colitis ◽

Chinese Medicine ◽

Traditional Chinese Medicine ◽

Disease Activity ◽

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Activity Index ◽

Disease Activity Index ◽

Therapeutic Effects ◽

Inflammatory Disorder

Plant-sourced formulations such as Iberogast and the traditional Chinese medicine formulation, Cmed, purportedly possess anti-inflammatory and radical scavenging properties. We investigated Iberogast and Cmed, independently, for their potential to decrease the severity of the large bowel inflammatory disorder, ulcerative colitis. Sprague Dawley rats (n = 8/group) received daily 1 mL gavages (days 0-13) of water, Iberogast (100 μL/200 μL), or Cmed (10 mg/20 mg). Rats ingested 2% dextran sulfate sodium or water ad libitum for 7 days commencing on day 5. Dextran sulfate sodium administration increased disease activity index scores from days 6 to 12, compared with water controls ( P < .05). On day 10, 200 μL Iberogast decreased disease activity index scores in colitic rats compared with colitic controls ( P < .05). Neither Iberogast nor Cmed achieved statistical significance for daily metabolic parameters or colonic crypt depth. The therapeutic effects of Iberogast and Cmed were minimal in the colitis setting. Further studies of plant extracts are required investigating greater concentrations and alternative delivery systems.

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Tanshinone IIA Protects against Dextran Sulfate Sodium- (DSS-) Induced Colitis in Mice by Modulation of Neutrophil Infiltration and Activation

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/7916763 ◽

2016 ◽

Vol 2016 ◽

pp. 1-10 ◽

Cited By ~ 8

Author(s):

Xiaowei Liu ◽

Haiyue He ◽

Tingting Huang ◽

Zhen Lei ◽

Fuquan Liu ◽

...

Keyword(s):

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Intestinal Inflammation ◽

Therapeutic Potential ◽

Activity Index ◽

Critical Role ◽

Neutrophil Migration ◽

Neutrophil Infiltration ◽

Tanshinone Iia

Neutrophils play a critical role in the initiation and maintenance of intestinal inflammation. However, conventional neutrophil-targeted therapies can impair normal host defense. Tanshinone IIA has been recently revealed to act directly on neutrophils. Hence, we aimed at investigating whether Tanshinone IIA can protect against experimental colitis through modulation of neutrophils. We induced colitis in C57BL/6 mice by giving 3% dextran sulfate sodium (DSS) orally, and meanwhile, we treated mice daily with Tanshinone IIA intraperitoneally. The severity of colitis was evaluated by calculating disease activity index (DAI) and histological parameters. Neutrophil infiltration and activation in the colons of mice were measured. Moreover, whether Tanshinone IIA has direct effects on neutrophil migration and activation was determined in vitro. Our data showed that Tanshinone IIA significantly ameliorated the severity of DSS-induced colitis in mice, evidenced by the reduced DAI and improved colonic inflammation. In addition, Tanshinone IIA decreased neutrophil infiltration of intestinal mucosa and activation and reduced colonic inflammatory cytokines in DSS-treated mice. Furthermore, Tanshinone IIA was demonstrated to significantly suppress neutrophil migration and activation. These results provide compelling evidence that Tanshinone IIA has a therapeutic potential for alleviating inflammatory colitis in mice, which is possibly mediated by the immunomodulation of neutrophils.

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Dietary Alaska Pollock Protein Attenuates the Experimental Colitis Induced by Dextran Sulfate Sodium via Regulation of Gut Microbiota and Its Metabolites in Mice

Metabolites ◽

10.3390/metabo12010044 ◽

2022 ◽

Vol 12 (1) ◽

pp. 44

Author(s):

Genki Tanaka ◽

Nozomi Hagihara ◽

Ryota Hosomi ◽

Takaki Shimono ◽

Seiji Kanda ◽

...

Keyword(s):

Gut Microbiota ◽

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Activity Index ◽

Body Weight Loss ◽

Disease Activity Index ◽

Experimental Colitis ◽

Short Chain Fatty Acids ◽

Spleen Weight ◽

Reduced Body

Protein derived from fish has not only nutritional properties but also health-promoting properties. Few studies have examined the effect of dietary Alaska pollock protein (APP) on the anticolitis effect reported to be associated with metabolic syndrome (MetS). This study investigated the effect of APP intake on colitis symptoms, gut microbiota, and its metabolites in the experimental colitis mouse model induced by dextran sulfate sodium (DSS). Male C57BL/6J mice were divided into three groups: (1) DSS-untreated mice fed an American Institute of Nutrition (AIN) 93G diet (protein source is casein), (2) DSS-treated mice fed an AIN93G diet, and (3) DSS-treated mice fed an APP diet. After the mice were fed the diets for 21 days, experimental colitis was induced by three cycles of 2% DSS administration for 5 days followed by washouts over the course of 5 days. APP-reduced body weight loss increased the disease activity index, and elevated spleen weight and alleviated colon length shortening and colonic tissue damage. Furthermore, APP altered the structure and composition of the microbiota and short-chain fatty acids in feces. Since APP intake alleviates experimental colitis induced by DSS administration through alterations in the gut microbiota and its metabolites, we deduced that APP would inhibit MetS progression via colitis suppression.

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Protective mechanisms of 6-gingerol in dextran sulfate sodium-induced chronic ulcerative colitis in mice

Human & Experimental Toxicology ◽

10.1177/0960327117751235 ◽

2018 ◽

Vol 37 (10) ◽

pp. 1054-1068 ◽

Cited By ~ 11

Author(s):

BO Ajayi ◽

IA Adedara ◽

EO Farombi

Keyword(s):

Ulcerative Colitis ◽

Drinking Water ◽

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Activity Index ◽

Biological Activities ◽

Disease Activity Index ◽

Aberrant Crypt Foci ◽

Necrosis Factor Alpha ◽

Monocyte Chemoattractant Protein 1

Ulcerative colitis (UC) is a relapsing and remitting inflammatory disease of the colon, with an increasing incidence worldwide. 6-Gingerol (6G) is a bioactive constituent of Zingiber officinale, which has been reported to possess various biological activities. This study was designed to evaluate the role of 6G in chronic UC. Chronic UC was induced in mice by three cycles of 2.5% dextran sulfate sodium (DSS) in drinking water. Each cycle consisted of 7 days of 2.5% DSS followed by 14 days of normal drinking water. 6G (100 mg/kg) and a reference anti-colitis drug sulfasalazine (SZ) (100 mg/kg) were orally administered daily to the mice throughout exposure to three cycles of 2.5% DSS. Administration of 6G and SZ significantly prevented disease activity index and aberrant crypt foci formation in DSS-treated mice. Furthermore, 6G and SZ suppresses immunoexpression of tumor necrosis factor alpha, interleukin-1β, inducible nitric oxide synthase, Regulated on activation, normal T cell expressed and secreted (RANTES), and Monocyte chemoattractant protein-1 (MCP-1) in the DSS-treated mice. 6G effectively protected against colonic oxidative damage by augmenting the antioxidant status with marked decrease in lipid peroxidation levels in DSS-treated mice. Moreover, 6G significantly inhibited nuclear factor kappa B (P65), p38, cyclooxygenase-2, and β-catenin whereas it enhanced IL-10 and adenomatous polyposis coli expression in DSS-treated mice. In conclusion, 6G prevented DSS-induced chronic UC via anti-inflammatory and antioxidative mechanisms and preservation of the Wnt/β-catenin signaling pathway.

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