scholarly journals EFFECT OF LUNASIN-RICH SOYBEAN EXTRACT UPON TNF-α EXPRESSION ON COLONIC EPITHELIAL CELLS OF MICE INDUCED BY AZOXYMETHANE/DEXTRAN SODIUM SULFATE

2019 ◽  
pp. 12-16
Author(s):  
KUSMARDI KUSMARDI ◽  
RENATA TAMARA ◽  
ARI ESTUNINGTYAS ◽  
ARYO TEDJO
Keyword(s):  
Epithelial Cells ◽  
Sodium Sulfate ◽  
Distal Colon ◽  
Positive Control ◽  
Negative Control ◽  
Dextran Sodium Sulfate ◽  
Colon Tissue ◽  
Colonic Epithelial Cells ◽  
Tnf Α ◽  
Soybean Extract

Objective: Colorectal cancer (CRC) contributes to 9.7% of all cancer, and its pathogenesis is related to chronic inflammation. However, current cancer therapy options are lacking, and peptide in food has become popular among researchers because it is cheap, easy to get, has a low toxicity, and is a promising cancer-preventing agent. This research aimed to investigate whether lunasin from soybeans can reduce the expression of pro-inflammatory cytokine TNF-α in colonic epithelial cells. Methods: Thirty Swiss Webster mice were randomly allocated to six groups. One group was normal, and in five groups, carcinogenesis was induced using azoxymethane (AOM) and dextran sodium sulfate (DSS). The mice were then given nothing (negative control), aspirin (positive control), and lunasin-rich soybean extract (LSE) in three different doses (250, 300, and 350 mg/kgBW) for four weeks. Distal colon tissue was immunohistochemically stained and then observed under a light microscope with 400X magnification to count epithelial cells, based on their color. The index was calculated using optical density scores. Results: LSE was shown to decrease the expression of tumor necrosis factor (TNF)-α. This decrease was statistically significant between the negative control and a dose of 300 mg/kgBW (p=0.016) and 350 mg/kgBW (p=0.009), yet it was not significant with a dose of 250 mg/kgBW (p=0.754). Conclusion: a dose of 300 mg/kgBW or higher of LSE can reduce the expression of TNF-α.

scholarly journals MiR-223 improves intestinal inflammation through inhibiting the IL-6/STAT3 signaling pathway in dextran sodium sulfate-induced experimental colitis

2020 ◽  
Author(s):  
Juanjuan Zhang ◽  
Chenyang Wang ◽  
Zhen Guo ◽  
Binlin Da ◽  
Weiming Zhu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Sodium Sulfate ◽  
Quantitative Polymerase Chain Reaction ◽  
Negative Control ◽  
Dextran Sodium Sulfate ◽  
Enzyme Linked Immunosorbent Assay ◽  
Colonic Inflammation ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Tnf Α

Abstract Background: The pathogenesis of inflammatory bowel disease (IBD) has not yet been clarified and is closely related to several proinflammatory factors. MicroRNA-233 (miR-223) might be involved in the development of IBD; however, the mechanism underlying its pathogenesis is unclear. In this study, we attempted to determine the role of miR-223 in dextran sodium sulfate (DSS)-induced colitis and explore the involvement of the IL-6/STAT3 pathway in the development of intestinal mucosal inflammation.Methods: Male C57BL/6 mice were divided into six groups: control (WT) group, DSS group, DSS+miR-223 agomir (DSS+A) group, DSS+miR-223 agomir negative control (DSS+A+NC) group, DSS+miR-223 antagomir (DSS+AN) group and DSS+miR-223 antagomir negative control (DSS+AN+NC) group. Body weight, stool consistency, fecal blood and the disease activity index (DAI) score were recorded daily. The length of each colon was measured, and colonic inflammation was evaluated with hematoxylin and eosin (H&E) staining and histopathological scoring. The expression of myeloperoxidase (MPO), TNF-α, IL-6, IL-10 and IL-17 in the colonic tissues was measured by Enzyme-linked Immunosorbent Assay (ELISA) and real-time quantitative polymerase chain reaction (RT-qPCR). The mRNA expression of gp130, Bcl-2 and Bcl-xl in the colon was measured using RT-qPCR. The colonic levels of STAT3 and p-STAT3 were determined by Western blotting.Results: MiR-223 expression in the terminal ileum and colon was increased in the DSS group compared with the WT group. Colitis symptoms were significantly alleviated in the DSS+A group and exacerbated in the DSS+AN group after administration of the miR-223 agomir and antagomir, respectively. MPO, TNF-α, IL-6 and IL-17 were decreased and IL-10 was increased in the DSS+A group, but these changes were reversed in the DSS+AN group. Gp130 mRNA, p-STAT3, Bcl-2 and Bcl-xl in the colon declined in the DSS+A group, but these levels increased in the DSS+AN group.Conclusion: The upregulation of miR-223 by agomir administration alleviated colonic inflammation in a DSS-induced colitis model, which was likely mediated by inhibiting the production of proinflammatory cytokines via the IL-6/STAT3 signaling pathway. These findings provide evidence that miR-223 might have potential therapeutic implications in IBD.

scholarly journals MUC2 Mucin and Butyrate Contribute to the Synthesis of the Antimicrobial Peptide Cathelicidin in Response to Entamoeba histolytica- and Dextran Sodium Sulfate-Induced Colitis

2017 ◽  
Vol 85 (3) ◽  
Author(s):  
Eduardo R. Cobo ◽  
Vanessa Kissoon-Singh ◽  
France Moreau ◽  
Ravi Holani ◽  
Kris Chadee
Keyword(s):  
Epithelial Cells ◽  
Antimicrobial Peptide ◽  
Entamoeba Histolytica ◽  
Sodium Sulfate ◽  
Mapk Signaling ◽  
Dextran Sodium Sulfate ◽  
Mitogen Activated Protein Kinase ◽  
Colonic Epithelial Cells ◽  
Content Type ◽  
Mucus Barrier

ABSTRACT Embedded in the colonic mucus are cathelicidins, small cationic peptides secreted by colonic epithelial cells. Humans and mice have one cathelicidin-related antimicrobial peptide (CRAMP) each, LL-37/hCAP-18 and Cramp, respectively, with related structure and functions. Altered production of MUC2 mucin and antimicrobial peptides is characteristic of intestinal amebiasis. The interactions between MUC2 mucin and cathelicidins in conferring innate immunity against Entamoeba histolytica are not well characterized. In this study, we quantified whether MUC2 expression and release could regulate the expression and secretion of cathelicidin LL-37 in colonic epithelial cells and in the colon. The synthesis of LL-37 was enhanced with butyrate (a product of bacterial fermentation) and interleukin-1β (IL-1β) (a proinflammatory cytokine in colitis) in the presence of exogenously added purified MUC2. The LL-37 responses to butyrate and IL-1β were higher in high-MUC2-producing cells than in lentivirus short hairpin RNA (shRNA) MUC2-silenced cells. Activation of cyclic adenylyl cyclase (AMP) and mitogen-activated protein kinase (MAPK) signaling pathways was necessary for the simultaneous expression of MUC2 and cathelicidins. In Muc2 mucin-deficient (Muc2 −/−) mice, murine cathelicidin (Cramp) was significantly reduced compared to that in Muc2 +/− and Muc2 +/+ littermates. E. histolytica-induced acute inflammation in colonic loops stimulated high levels of cathelicidin in Muc2 +/+ but not in Muc2 −/− littermates. In dextran sodium sulfate (DSS)-induced colitis in Muc2 +/+ mice, which depletes the mucus barrier and goblet cell mucin, Cramp expression was significantly enhanced during restitution. These studies demonstrate regulatory mechanisms between MUC2 and cathelicidins in the colonic mucosa where an intact mucus barrier is essential for expression and secretion of cathelicidins in response to E. histolytica- and DSS-induced colitis.

ANTI-INFLAMMATORY EFFECT OF ETHANOL EXTRACT OF MAHKOTA DEWA [PHALERIA MACROCARPA (SCHEFF. BOERL)] LEAVES IN MOUSE COLITIS INDUCED BY AZOXYMETHANE (AOM) AND DEXTRAN SODIUM SULFATE (DSS): FOCUS ON RECTAL TISSUE

2020 ◽  
pp. 106-110
Author(s):  
AFID BRILLIANA PUTRA ◽  
KUSMARDI KUSMARDI ◽  
ARYO TEDJO ◽  
ARI ESTUNINGTYAS ◽  
MUHAMMAD ILHAM DHIYA RAKASIWI
Keyword(s):  
Sodium Sulfate ◽  
Ethanol Extract ◽  
Goblet Cells ◽  
Positive Control ◽  
Negative Control ◽  
Dextran Sodium Sulfate ◽  
Glass Slides ◽  
Phaleria Macrocarpa ◽  
Colitis Model

Objective: In this study, we aim to analyze the effect of this ethanol extract on the average number of goblet cells per crypt, number of inflammatory foci and number of angiogenesis in the rectal tissues of mice colitis-model that induced by azoxymethane (AOM) and dextran sodium sulfate (DSS). Methods: This study was carried out by experimental in vivo using Balb/c mice. The mice were divided into five groups of treatment: normal, negative control (AOM/DSS), positive control (AOM/DSS+aspirin), EMD25 (AOM/DSS+25% ethanol extract) and EMD12.5 (AOM/DSS+12.5% ethanol extract). The mice were euthanized and their rectal tissues were placed on glass slides for histopathological observation using haematoxylin–eosin staining. Results: The administration of the ethanol extract of mahkota dewa (Phaleria macrocarpa) leaves cannot inhibit the decrease in the average number of goblet cells per crypt (p=0.450) and cannot reduce the number of inflammation foci (p=0.146) and the number of angiogenesis (p=0.728). The ethanol extract of mahkota dewa (Phaleria macrocarpa) leaves could not inhibit the inflammation induced by AOM/DSS in the rectal tissues of mice. However, the extract has a tendency to maintain the average number of goblet cells per crypt. Conclusion: Ethanol extract of Mahkota Dewa leaves can inhibit inflammation in mice's rectal tissue.

scholarly journals Ethanol Extract ofCordyceps militarisGrown on Germinated Soybeans Attenuates Dextran-Sodium-Sulfate- (DSS-) Induced Colitis by Suppressing the Expression of Matrix Metalloproteinases and Inflammatory Mediators

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Dong Ki Park ◽  
Hye-Jin Park
Keyword(s):  
Matrix Metalloproteinases ◽  
Inflammatory Mediators ◽  
Sodium Sulfate ◽  
Activity Index ◽  
Disease Activity Index ◽  
Ethanol Extract ◽  
Treated Group ◽  
Dextran Sodium Sulfate ◽  
Protective Agent ◽  
Colon Tissue

The effect ofCordyceps militaris(CM) grown on germinated soybeans (GSC) in the inflammatory bowel disease (IBD) model was studied. To demonstrate the preventive effect of GSC extract in a dextran-sodium-sulfate- (DSS-) induced acute colitis mouse model, GSC was administered 2 days before DSS coadministration. GSC significantly suppressed DSS-induced disease activity index (DAI) as well as histopathological scores, compared to control or CM-treated group. To elucidate the anti-IBD activity of GSC, we checked the level of matrix metalloproteinases (MMPs) and inflammatory mediators. GSC extract decreased the level of MMP-3 and -9 mRNAs and p53 proteins. The level and activity of LPS-induced MMP-9 were reduced in GSC-treated RAW264.7 cells. It also attenuated the level of inducible nitric oxide synthase (iNOS) and tumor necrosis factor- (TNF-)αmRNAs both in colon tissue and in macrophage cells. These results suggest that GSC can be applied as a protective agent against IBDs.

scholarly journals EKSPRESI Tumor Necrosis Factor alpha (TNF-α) DAN Transforming growth factors beta (TGF-β) PADA PERIODONTITIS APIKALIS KRONIS AKIBAT INDUKSI Enterococcus faecalis PADA TIKUS WISTAR

2019 ◽  
Vol 7 (2) ◽  
pp. 66
Author(s):  
Richard Fritzgerald ◽  
Cecilia Lunardhi ◽  
Ruslan Effendy ◽  
Tamara Yuanita
Keyword(s):  
Tissue Damage ◽  
Treated Group ◽  
Positive Control ◽  
Negative Control ◽  
Control Group ◽  
Transforming Growth Factors ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Background. Root canal treatment is a main role in decreasing infection from root canal and pulp. The main cause of periapical damage mostly are bacteries. E.faecalis is a bactery that is found as an etiology of endodontic treatment failure. Cell wall of this bacteria is containing Lipoteichoic acid (LTA). LTA can penetrate into the periradicular tissue, act as endotoxin in host and cause periradicular inflammation then lead to bone destruction. LTA stimulates immunology reaction that produce Tumor Necrosis Factor alpha (TNF-α) and Transforming growth factors beta (TGF-ß). TNF-α is a main mediator and also have an important role in inflamation response otherwise TGF-ß is working as a multifunction  regulator of cell growth and differentiation during reforming and remodelling.  Purpose. The aim of this study is to know about the expression of TNF-α and TGF-ß during the periapical tissue damage due to induction of E.faecalis. Method. This study used laboratory experimental with the post test only control group design. A total of 30 male rats were randomly divided into 3 main groups, Group A (control negative) : normal tooth. Group B (control positive) : every tooth was induced only by sterile BHI-b. Group C (treated group) : every tooth  was induced by 10 μl BHI-b E.faecalis ATCC212(106 CFU). The animals were sacrificed 21 days later and prepared for histological examination of tissue damage, then we did the immunohistochemistry  followed by calculation on the light microscope. Result. The analysis revealed that the expression of TNF-α at treated group are higher than negative control and positive control but the expression of  TGF-ß at treated group are higher than the negative control group but lower than positive control. Conclusion. From this study we know that the expression of TNF-α and TGF-ß are changing during the periapical tissue damage that induced by E.faecalis.

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