Potential of Phaleria macrocarpa Leaves Ethanol Extract to Upregulate the Expression of Caspase-3 in Mouse Distal Colon after Dextran Sodium Sulphate Induction

Objective: To demonstrates the ability of P. macrocarpa leaf extract to reduce inflammation of the distal colon in DSS/AOM-induced mice. Methods: In vivo experimental research using Balb/c mice induced by 0.2 ml azoxymethane (AOM) 0.1% once and 1% dextran sodium sulphate (DSS) for one week; additionally, ethanol extract of P. macrocarpa leaves, 25 mg and 50 mg, and 0.84 mg acetosal were given orally. The mice were sacrificed after 20 w. Histopathological examination (hematoxylin-eosin staining) was conducted by counting the average number of goblet cells per crypt, inflammatory focus and angiogenesis. Results: Ethanol extract of P. macrocarpa leaves was able to prevent the decrease in the number of goblet cells (p<0.05). However, the administration of ethanol P. macrocarpa leaf extract could not reduce focal inflammation and angiogenesis in inflammation of the distal colon. Conclusion: Ethanol extract of the Mahkota Dewa leaves is able to prevent inflammation of the distal colon by preventing the decrease in the number of goblet cells.

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Inhibitory Activity Goblet Depletion and focal inflammatory Phaleria macrocarpha Leaves Ethanol Extract on Crypta Mouse after Dextran Sodium Sulphate Induction

International Journal of PharmTech Research ◽

10.20902/ijptr.2019.120106 ◽

2019 ◽

Vol 12 (01) ◽

pp. 37-48

Author(s):

Rianti Maharani ◽

Kusmardi ◽

Berna Elya

Keyword(s):

Inhibitory Activity ◽

Ethanol Extract ◽

Sodium Sulphate ◽

Dextran Sodium Sulphate

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Diminished nitroprusside-induced relaxation of inflamed colonic smooth muscle in mice

Mediators of Inflammation ◽

10.1080/09629359890974 ◽

1998 ◽

Vol 7 (4) ◽

pp. 283-287 ◽

Cited By ~ 13

Author(s):

J. D. van Bergeijk ◽

H. van Westreenen ◽

P. Adhien ◽

F. J. Zijlstra

Keyword(s):

Nitric Oxide ◽

Smooth Muscle ◽

Muscle Contraction ◽

Regional Differences ◽

Distal Colon ◽

Smooth Muscle Contraction ◽

Sodium Sulphate ◽

Nitric Oxide Donor ◽

Colonic Tissue ◽

Dextran Sodium Sulphate

The dextran sodium sulphate (DSS) induced colitis in mice was used as a experimental model to study the contractility of murine longitudinal colonic smooth muscle during inflammation. Smooth muscle segments of proximal, middle and distal colon were mounted in organ baths . Smooth muscle contraction was induced by carbachol, showing an aboral increase in activity, where as in the inflamed middle colonics egment a marked decr ease in activity was observed. The dilatative effect of sodium-nitroprus -side (SNP) as a nitric oxide donor was investigated after precontraction by carbachol. Both in normal and DSS segments administration of SNP to isolated mouse colonic smooth muscle preparations caused regional differences in relaxation, the highest relaxation seen in normal proximal colonic tissue. However, this relaxation was markedly reduced in inflamed proximal preparations , associated with a diminished cGMP contents .

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Potential Inhibition by Phaleria macrocarpa Leaves Ethanol Extract on Ki-67 Expression in Distal Colon Mouse

Pharmacognosy Journal ◽

10.5530/pj.2021.13.56 ◽

2020 ◽

Vol 13 (2) ◽

pp. 443-449

Author(s):

Kusmardi Kusmardi ◽

Elvan Wiyarta ◽

Ari Estuningtyas ◽

Nurhuda Sahar ◽

Yurnadi Hanafi Midoen ◽

...

Keyword(s):

Ethanol Extract ◽

Distal Colon ◽

Ki 67 ◽

Phaleria Macrocarpa

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The Effect of Ethanol Extract Turmeric Rhizome (Curcuma Longa) to Histologycal Structure of Rat Rectum Induced Dextran Sodium Sulphate (DSS)

Jurnal ILMU DASAR ◽

10.19184/jid.v20i1.7629 ◽

2019 ◽

Vol 20 (1) ◽

pp. 13

Author(s):

Lidia Maziyyatun Nikmah ◽

Susantin Fajariyah ◽

M. Mahriani

Keyword(s):

Goblet Cell ◽

Curcuma Longa ◽

Ethanol Extract ◽

Negative Control Group ◽

Negative Control ◽

Sodium Sulphate ◽

Control Group ◽

Dextran Sodium Sulphate ◽

Anti Inflammatory ◽

Group 1

Turmeric (Curcuma longa) is a plant that people use as a traditional medicine to treat some diseases such as: anti-inflammatory, antidiarrhea, antioxidants, hepatoprotector, and others. One of the main chemical compounds contained in turmeric and has a role as anti-inflammatory is curcumin. This study was conducted to determine the effect of ethanol extract of turmeric rhizome (Curcuma longa) on the histologycal structure of rat rectum induced by Dextran Sodium Sulphate (DSS). Wistar strain rats was divided into three groups: negative control group, positive control group (1% DSS), and DSS treatment group 1% + ethanol extract of turmeric rhizome dose 200mg/KgBB. DSS is given ad libitum, while ethanol extract of turmeric rhizome is given orally. We used paraffin method and Haematoxilyn Eosin staining to make the preparation organ. The data were analyzed using One Way ANOVA test, Duncan Multiple Range Test (DMRT) test, and correlation test. The result of this study is DSS administration has an effect on decreasing average of crypt, number of Goblet cell, and depletion of rectal mucous layer. While treatment of extract turmeric rhizome can increase height of crypt and number of Goblet cell in rectal mucosal layer of rat. Keywords: Exctract of turmeric rhizome, DSS, rectum, Rattus norvegicus

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Dietary folate does not significantly affect the intestinal microbiome, inflammation or tumorigenesis in azoxymethane–dextran sodium sulphate-treated mice

British Journal Of Nutrition ◽

10.1017/s0007114512001857 ◽

2012 ◽

Vol 109 (4) ◽

pp. 630-638 ◽

Cited By ~ 16

Author(s):

Amanda J. MacFarlane ◽

Nathalie A. Behan ◽

Fernando M. G. Matias ◽

Judy Green ◽

Don Caldwell ◽

...

Keyword(s):

Colon Cancer ◽

Distal Colon ◽

Sodium Sulphate ◽

Intestinal Microbiome ◽

Dextran Sodium Sulphate ◽

Dietary Folate ◽

Chemically Induced ◽

Inflammatory Bowel ◽

Tumour Initiation ◽

The Impact

Inflammatory bowel disease (IBD) is a risk factor for the development of colon cancer. Environmental factors including diet and the microflora influence disease outcome. Folate and homocysteine have been associated with IBD-mediated colon cancer but their roles remain unclear. We used a model of chemically induced ulcerative colitis (dextran sodium sulphate (DSS)) with or without the colon carcinogen azoxymethane (AOM) to determine the impact of dietary folic acid (FA) on colonic microflora and the development of colon tumours. Male mice (n 15 per group) were fed a FA-deficient (0 mg/kg), control (2 mg/kg) or FA-supplemented (8 mg/kg) diet for 12 weeks. Folate status was dependent on the diet (P< 0·001) and colitis-induced treatment (P= 0·04) such that mice with colitis had lower circulating folate. FA had a minimal effect on tumour initiation, growth and progression, although FA-containing diets tended to be associated with a higher tumour prevalence in DSS-treated mice (7–20 v. 0 %, P= 0·08) and the development of more tumours in the distal colon of AOM-treated mice (13–83 % increase, P= 0·09). Folate deficiency was associated with hyperhomocysteinaemia (P< 0·001) but homocysteine negatively correlated with tumour number (r − 0·58, P= 0·02) and load (r − 0·57, P= 0·02). FA had no effect on the intestinal microflora. The present data indicate that FA intake has no or little effect on IBD or IBD-mediated colon cancer in this model and that hyperhomocysteinaemia is a biomarker of dietary status and malabsorption rather than a cause of IBD-mediated colon cancer.

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Faculty Opinions recommendation of Helicobacter pylori DNA decreases pro-inflammatory cytokine production by dendritic cells and attenuates dextran sodium sulphate-induced colitis.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.10005956.14859111 ◽

2012 ◽

Author(s):

Steven Moss ◽

Songhua Zhang

Keyword(s):

Helicobacter Pylori ◽

Dendritic Cells ◽

Inflammatory Cytokine ◽

Cytokine Production ◽

Sodium Sulphate ◽

Dextran Sodium Sulphate ◽

Inflammatory Cytokine Production

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Titanium Dioxide Presents a Different Profile in Dextran Sodium Sulphate-Induced Experimental Colitis in Mice Lacking the IBD Risk Gene Ptpn2 in Myeloid Cells

International Journal of Molecular Sciences ◽

10.3390/ijms22020772 ◽

2021 ◽

Vol 22 (2) ◽

pp. 772

Author(s):

Javier Conde ◽

Marlene Schwarzfischer ◽

Egle Katkeviciute ◽

Janine Häfliger ◽

Anna Niechcial ◽

...

Keyword(s):

Bone Marrow ◽

Titanium Dioxide ◽

Genetic Risk ◽

Intestinal Inflammation ◽

Sodium Sulphate ◽

Food Additive ◽

Wild Type ◽

Dextran Sodium Sulphate ◽

Risk Gene ◽

The Impact

Environmental and genetic factors have been demonstrated to contribute to the development of inflammatory bowel disease (IBD). Recent studies suggested that the food additive; titanium dioxide (TiO2) might play a causative role in the disease. Therefore, in the present study we aimed to explore the interaction between the food additive TiO2 and the well-characterized IBD risk gene protein tyrosine phosphatase non-receptor type 2 (Ptpn2) and their role in the development of intestinal inflammation. Dextran sodium sulphate (DSS)-induced acute colitis was performed in mice lacking the expression of Ptpn2 in myeloid cells (Ptpn2LysMCre) or their wild type littermates (Ptpn2fl/fl) and exposed to the microparticle TiO2. The impact of Ptpn2 on TiO2 signalling pathways and TiO2-induced IL-1β and IL-10 levels were studied using bone marrow-derived macrophages (BMDMs). Ptpn2LysMCre exposed to TiO2 exhibited more severe intestinal inflammation than their wild type counterparts. This effect was likely due to the impact of TiO2 on the differentiation of intestinal macrophages, suppressing the number of anti-inflammatory macrophages in Ptpn2 deficient mice. Moreover, we also found that TiO2 was able to induce the secretion of IL-1β via mitogen-activated proteins kinases (MAPKs) and to repress the expression of IL-10 in bone marrow-derived macrophages via MAPK-independent pathways. This is the first evidence of the cooperation between the genetic risk factor Ptpn2 and the environmental factor TiO2 in the regulation of intestinal inflammation. The results presented here suggest that the ingestion of certain industrial compounds should be taken into account, especially in individuals with increased genetic risk

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