scholarly journals Dynamic evaluation of ulcerative colitis model in BALB/c mice induced by dextran sulfate sodium salt

2021 ◽  
Author(s):  
Xu YS ◽  
M Tang ◽  
Q Lu ◽  
H Ahunova ◽  
ZHILIN JIANG
Keyword(s):  
Ulcerative Colitis ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Activity Index ◽  
Disease Activity Index ◽  
Mucosal Injury ◽  
New Drugs ◽  
T Cell Subsets ◽  
Intragastric Administration ◽  
Injury Index

Abstract In this experiment, BALB/c mice were induced by dextran sulfate sodium (DSS) to establish ulcerative colitis (UC) model. Treatment by intragastric administration of oxalazine (600 mg/Kg)，the disease activity index (DAI), colonic mucosal injury index (CMDI) and histopathological score (HS) of mice in each group were measured at different times. And the changes of T cell subsets in spleen and the content of IL-1 β in serum of UC mice at different time points were detected by flow cytometry and ELISA method. The investigation of the dynamic changes of various indexes in mice during the period of modeling and administration is of great significance for exploring the etiology and pathological changes of the disease, determining the methods of treatment and the research and development of new drugs.

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

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.

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

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).

scholarly journals EGCG Maintains Th1/Th2 Balance and Mitigates Ulcerative Colitis Induced by Dextran Sulfate Sodium through TLR4/MyD88/NF-κB Signaling Pathway in Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Xue Bing ◽  
Liu Xuelei ◽  
Dong Wanwei ◽  
Liang Linlang ◽  
Chen Keyan
Keyword(s):  
Ulcerative Colitis ◽  
Flow Cytometry ◽  
Protective Effect ◽  
Signaling Pathway ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Activity Index ◽  
Mucosal Injury ◽  
Inflammatory Factors ◽  
Intestinal Mucosal Injury

Objective. To observe the protective effect of epigallocatechin gallate (EGCG) on dextran sulfate sodium- (DSS-) induced ulcerative colitis in rats and to explore the roles of TLR4/MyD88/NF-κB signaling pathway. Methods. Rat models of ulcerative colitis were established by giving DSS. EGCG (50 mg/kg/d) was given to assess disease activity index. HE staining was applied to observe histological changes. ELISA and qPCR detected the expression of inflammatory factors. Flow cytometry was used to measure the percentage of CD4+IFN-γ+ and CD4+IL-4+ in the spleen and colon. TLR4 antagonist E5564 was given in each group. Flow cytometry was utilized to detect CD4+IFN-γ+ and CD4+IL-4+ cells. Immunohistochemistry, qPCR, and western blot assay were applied to measure the expression of TLR4, MyD88, and NF-κB. Results. EGCG improved the intestinal mucosal injury in rats, inhibited production of inflammatory factors, maintained the balance of Th1/Th2, and reduced the expression of TLR4, MyD88, and NF-κB. After TLR4 antagonism, the protective effect of EGCG on intestinal mucosal injury was weakened in rats with ulcerative colitis, and the expressions of inflammatory factors were upregulated. Conclusion. EGCG can inhibit the intestinal inflammatory response by reducing the severity of ulcerative colitis and maintaining the Th1/Th2 balance through the TLR4/MyD88/NF-κB signaling pathway.

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

2013 ◽  
Vol 19 (1) ◽  
pp. 10-19 ◽  
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.

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

2018 ◽  
Vol 37 (10) ◽  
pp. 1054-1068 ◽  
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.

scholarly journals Preventive Effect of Cardiotrophin-1 Administration before DSS-Induced Ulcerative Colitis in Mice

2019 ◽  
Author(s):  
Ana I Sanchez-Garrido ◽  
Vanessa Prieto-Vicente ◽  
Victor Blanco-Gozalo ◽  
Miguel Arevalo ◽  
Yaremi Quiros ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Clinical Course ◽  
Activity Index ◽  
Disease Activity Index ◽  
Histological Damage ◽  
Current Therapies ◽  
Histology And Immunohistochemistry

Ulcerative colitis (UC) is a relatively frequent, chronic disease that impacts significantly the patient&rsquo;s quality of life. Although many therapeutic options are available, additional approaches are needed because many patients either do not respond to current therapies or show significant side effects. Cardiotrophin-1 (CT-1) is a cytokine with potent cytoprotective, anti-inflammatory, and antiapoptotic properties. The purpose of this study was to assess if the administration of CT-1 could reduce colon damage in mice with experimental UC. UC was induced with 5% dextran sulfate sodium (DSS) in the drinking water. Some mice received i.v. dose of CT-1 (200 &micro;g/kg) 2 hours before and 2 and 4 days after DSS administration. Animals were followed during 7 days after DSS. The severity of UC was measured by standard scores. Colon damage was assessed by histology and immunohistochemistry. Inflammatory mediators were measured by Western blot and PCR. CT-1 administration to DSS-treated mice ameliorated both the clinical course (disease activity index), histological damage, inflammation (colon expression of TNF-&alpha;, IL-17, IL-10, INF-&gamma;, and iNOS), and apoptosis. Our results suggest that CT-1 administration before UC induction improves the clinical course, tissue damage and inflammation degree in DSS-induced UC in mice.

scholarly journals Atractylodin Attenuates Dextran Sulfate Sodium-Induced Colitis by Alleviating Gut Microbiota Dysbiosis and Inhibiting Inflammatory Response Through the MAPK Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Linghang Qu ◽  
Xiong Lin ◽  
Chunlian Liu ◽  
Chang Ke ◽  
Zhongshi Zhou ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Intestinal Inflammation ◽  
Mapk Pathway ◽  
Activity Index ◽  
Intestinal Barrier ◽  
Disease Activity Index ◽  
Inflammatory Factors ◽  
Therapeutic Effects

In this study, we investigated the therapeutic effects and mechanism of atractylodin (ATL) on dextran sulfate sodium (DSS)-induced ulcerative colitis in mice. We found that atractylodin could significantly reverse the effects of DSS-induced ulcerative colitis, such as weight loss, disease activity index score; shorten the colon length, and reverse the pathological changes in the colon of mice. Atractylodin could inhibit the activation of colonic macrophages by inhibiting the MAPK pathway and alleviate intestinal inflammation in the mouse model of ulcerative colitis. Moreover, it could protect the intestinal barrier by inhibiting the decrease of the tight junction proteins, ZO-1, occludin, and MUC2. Additionally, atractylodin could decrease the abundance of harmful bacteria and increase that of beneficial bacteria in the intestinal tract of mice, effectively improving the intestinal microecology. In an LPS-induced macrophage model, atractylodin could inhibit the MAPK pathway and expression of the inflammatory factors of macrophages. Atractylodin could also inhibit the production of lactate, which is the end product of glycolysis; inhibit the activity of GAPDH, which is an important rate-limiting enzyme in glycolysis; inhibit the malonylation of GAPDH, and, thus, inhibit the translation of TNF-α. Therefore, ours is the first study to highlight the potential of atractylodin in the treatment of ulcerative colitis and reveal its possible mechanism.

scholarly journals Anti-Inflammatory Effects of Heritiera littoralis Fruits on Dextran Sulfate Sodium- (DSS-) Induced Ulcerative Colitis in Mice by Regulating Gut Microbiota and Suppressing NF-κB Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-20
Author(s):  
Guosheng Lin ◽  
Minyao Li ◽  
Nan Xu ◽  
Xiaoli Wu ◽  
Jingjing Liu ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Gut Microbiota ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Activity Index ◽  
Disease Activity Index ◽  
Rrna Gene ◽  
Chemical Compositions ◽  
Protective Effects ◽  
Esi Ms

Aim of the Study. This study is aimed at exploring the effects and pharmacological mechanisms of the extracts from the Heritiera littoralis fruit (EFH) on dextran sulfate sodium- (DSS-) induced ulcerative colitis (UC) in mice. Materials and Methods. The chemical compositions of EFH were identified using LC-ESI-MS. The mice with 3% DSS-induced UC were administered EFH (200, 400, and 800 mg/kg), sulfasalazine (SASP, 200 mg/kg), and azathioprine (AZA, 13 mg/kg) for 10 days via daily gavage. The colonic inflammation was evaluated by the disease activity index (DAI), colonic length, histological scores, and levels of inflammatory mediators. The gut microbiota was characterized by 16S rRNA gene sequencing and analysis. Results. LC-ESI-MS analysis showed that EFH was rich in alkaloids and flavones. The results indicated that EFH significantly improved the DAI score, relieved colon shortening, and repaired pathological colonic variations in colitis. In addition, proteins in the NF-κB pathway were significantly inhibited by EFH. Furthermore, EFH recovered the diversity and balance of the gut microbiota. Conclusions. EFH has protective effects against DSS-induced colitis by keeping the balance of the gut microbiota and suppressing the NF-κB pathway.

scholarly journals Fermentation products of Danshen relieved dextran sulfate sodium-induced experimental ulcerative colitis in mice

2021 ◽  
Author(s):  
Le Su ◽  
Yue Su ◽  
Zaiyong An ◽  
Ping Zhang ◽  
Qiulin Yue ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Activity Index ◽  
Lactobacillus Rhamnosus ◽  
Public Health Problem ◽  
Disease Activity Index ◽  
Global Public Health ◽  
Biological Drugs ◽  
Fermentation Products

Abstract With the increased incidence and recognition, ulcerative colitis (UC) has become a global public health problem in the world. Although many immunosuppressants and biological drugs have been used for UC treatment, the cure rate is still very low. It is necessary to find some safe and long-term used medicine for UC cure. In recent years, fermented Chinese medicine has been more and more used in the treatments of inflammatory and chronic diseases. In this manuscript, Lactobacillus Rhamnosus (F-B4-1) and Bacillus Subtillis Natto (F-A7-1) were selected to ferment enzymatic Danshen. The fermented Danshen products were gavaged in the dextran sulfate sodium (DSS)-induced UC model mice. It is suggested that after fermented Danshen with Rhamnosus and then with Natto, Danshen had the better results to attenuate symptom of DSS-induced UC. It reduced the loss of body weight and disease activity index (DAI) and inhibited the abnormally short colon lengths and the colonic damage. Moreover, it suppressed pro-inflammatory cytokine expression during DSS-induced UC. The results indicated that fermented Danshen relieved DSS-induced UC in mice. And the Danshen fermented by probiotics might be an effective drug to treat UC in the clinic in the future.

scholarly journals β-Glucan Extracted from Highland Barley Alleviates Dextran Sulfate Sodium-Induced Ulcerative Colitis in C57BL/6J Mice

Molecules ◽  
2021 ◽  
Vol 26 (19) ◽  
pp. 5812
Author(s):  
Minjie Chen ◽  
Shuhua Tian ◽  
Shichao Li ◽  
Xinyi Pang ◽  
Jing Sun ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Activity Index ◽  
Intestinal Flora ◽  
Disease Activity Index ◽  
Gastrointestinal Dysfunction ◽  
Genes Encoding ◽  
Inflammatory Bowel ◽  
Highland Barley

Inflammatory bowel disease (IBD), which significantly affects human health, has two primary presentations: Crohn’s disease and ulcerative colitis (UC). Highland barley is the most common food crop for Tibetans and contains much more β-glucan than any other crop. Highland barley β-glucan (HBBG) can relieve the gastrointestinal dysfunction and promote intestines health. This study aimed to evaluate whether HBBG can relieve UC in mice. A mouse model of UC was established by adding 2% dextran sulfate sodium (DSS) to drinking water for 1 week. UC was alleviated after the introduction of the HBBG diet, as indicated by reductions in the disease activity index (DAI) score, histopathological damage, and the concentration of colonic myeloperoxidase (MPO), along with an improvement in colonic atrophy. Furthermore, we found that HBBG can increase the relative transcriptional levels of genes encoding ZO-1, claudin-1, occludin, and mucin2 (MUC2), thereby reducing intestinal permeability. Additionally, HBBG maintained the balance of proinflammatory and anti-inflammatory cytokines and modulated the structure of the intestinal flora.

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