scholarly journals Umbelliferone ameliorates ulcerative colitis induced by acetic acid via modulation of TLR4/NF-κB-p65/iNOS and PPARγ/SIRT1 signaling pathways in rats

2021 ◽  
Author(s):  
Basel A Abdel-Wahab ◽  
Saad A Alkahtani ◽  
Abdulsalam A Alqahtani ◽  
Emad H.M. Hassanein
Keyword(s):  
Ulcerative Colitis ◽  
Acetic Acid ◽  
Inflammatory Response ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Therapeutic Potential ◽  
Tissue Injury ◽  
Oxidative Injury ◽  
Control Group ◽  
Anti Inflammatory

Abstract Ulcerative colitis (UC) is a common chronic, idiopathic inflammatory bowel disease associated with inflammatory perturbation and oxidative stress. Umbelliferone (UMB) is a potent anti-inflammatory and antioxidant coumarin derivative. Depending on the possible mechanisms, we aimed to explore and elucidate the therapeutic potential of UMB on UC-inflammatory response and oxidative injury-induced via intrarectal administration of acetic acid (AA). Rats were assigned into four groups: control group, UMB (30 mg/kg) treated group, colitis model group (2 ml of AA; 3% v/v), and colitis treated with UMB groups. Our results exhibited that UMB improved macroscopic and histological tissue injury caused by the AA. Mechanistically, UMB reduced the elevated TNF-α, IL-6, MPO and VCAM-1 via effective downregulation of TLR-4, NF-κB and iNOS signaling pathway, thereby mediated potent anti-inflammatory effects. Moreover, UMB administration resulted in effective up-regulation of both PPARγ and SIRT1 signaling pathways, thereby inhibited both oxidative injury and inflammatory response. Conclusively, UMB protected against AA-induced UC in rats through suppressing of the TLR4/NF-κB-p65/iNOS signaling pathway and promoting the PPARγ/SIRT1 signaling. Indeed, our data proved the effectiveness of UMB in UC and introduced it as a potential therapeutic beneficial applicant for clinical application.

scholarly journals Protective Effect of Methane-Rich Saline on Acetic Acid-Induced Ulcerative Colitis via Blocking the TLR4/NF-κB/MAPK Pathway and Promoting IL-10/JAK1/STAT3-Mediated Anti-inflammatory Response

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Guanghui Wang ◽  
Bing Xu ◽  
Feiyu Shi ◽  
Mengfan Du ◽  
Yaguang Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ulcerative Colitis ◽  
Acetic Acid ◽  
Inflammatory Response ◽  
Protective Effect ◽  
Signaling Pathway ◽  
Tissue Damage ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Anti Inflammatory

Ulcerative colitis (UC) is an inflammation-related disease involved in uncontrolled inflammation and oxidative stress and is characterized by high recurrence and relapse risk. As a rising star in gas medicine, methane owns the properties of anti-inflammation, antioxidation, and antiapoptosis. Based on the possible mechanism, we aimed to investigate the effect of methane on UC. Methane-rich saline (MRS) was introduced here, and UC was induced by acetic acid. All the C57BL/6 mice were allocated into groups as follows: control group, colitis model group, colitis treated with salazosulfapyridine (SASP) group, and colitis treated with MRS (1 or 10 ml/kg) groups. Tissue damage, the degree of inflammation, oxidative stress, and apoptosis were evaluated in the study, as well as the TLR4/NF-κB/MAPK and IL-10/JAK1/STAT3 signaling pathways for further exploration of the potential mechanism. The results showed that MRS (1) alleviated tissue damage caused by acetic acid, (2) controlled acetic acid-induced inflammation, (3) inhibited acetic acid-caused oxidative stress, (4) reduced colonic cell apoptosis due to acetic acid, (5) suppressed the TLR-4/NF-κB/MAPK signaling pathway, and (6) activated IL-10/JAK1/STAT3 anti-inflammatory response to improve the injury induced by acetic acid. We conclude that MRS has a protective effect on acetic acid-induced ulcerative colitis in mice via blocking the TLR4/NF-κB/MAPK signaling pathway and promoting the IL-10/JAK1/STAT3-mediated anti-inflammatory response.

scholarly journals Anti-inflammatory effects of nicotine

2015 ◽  
Vol 18 (1) ◽  
pp. 5-12
Author(s):  
Corina-Daniela Ene ◽  
◽  
Mircea Penescu ◽  
Ilinca Nicolae ◽  
Emanoil Ceauşu ◽  
...  
Keyword(s):  
Experimental Data ◽  
Inflammatory Response ◽  
Signaling Pathways ◽  
Nicotinic Receptors ◽  
Inflammatory Process ◽  
Therapeutic Potential ◽  
Inflammatory Cells ◽  
Nicotinic Agonists ◽  
Anti Inflammatory ◽  
Stimulation Of

A number of epidemiological and experimental data have shown that nicotine stimulates anti-inflammatory response in extraneuronal tissues, response mediated by homopentameric nicotinic receptors, 7nAChR- alpha. The receptors are located mainly on immune and inflammatory cells. These pharmacological mechanisms, through which inflammatory process could be adjusted is the use of selective nicotinic agonists and antagonists, called anti-inflammatory. Treatment with nicotine initiates a series of intracellular events associated with stimulation of several signaling pathways: NFkB, JAK/STAT, MyD88/TLRs, MAPKs/ERKs. Knowledge of anti-inflammatory mechanisms mediated by alpha7nAChR is useful for valuing the therapeutic potential of nicotine in regulating the inflammatory response in certain pathological processes.

scholarly journals Efficacy of quercetin derivatives in prevention of ulcerative colitis in rats

2013 ◽  
Vol 6 (1) ◽  
pp. 9-12 ◽  
Author(s):  
Ruzena Sotnikova ◽  
Viera Nosalova ◽  
Jana Navarova
Keyword(s):  
Ulcerative Colitis ◽  
Acetic Acid ◽  
Intestinal Inflammation ◽  
Tissue Injury ◽  
Reductase Activity ◽  
Antioxidant Properties ◽  
Control Group ◽  
Wall Thickening ◽  
Quercetin Derivatives

Abstract Reactive oxygen species has been implicated to contribute significantly to tissue injury associated with ulcerative colitis. Thus compounds with antioxidant properties could be potential therapeutic agents in this disease. Flavonoid compounds are known to possess antioxidative and antiinflammatory properties. Two derivatives of the flavonoid quercetin (Q), chloronaphthoquinone quercetin (CNC) and monochloropivaloyl quercetin (MCP), showed improved antioxidant properties and moreover, they efficiently inhibited aldose reductase activity in vitro. The aim of the work was to test the potential efficacy of quercetin and these synthetic derivatives in vivo in prevention of intestinal inflammation during ulcerative colitis in rats. Colitis was induced by intracolonic administration of acetic acid (4% solution). The control group received the same volume of saline. The vehicle dimethyl sulfoxide (DMSO) and the drugs Q, CNC or MCP were administered orally two hours and then one hour before the acetic acid or saline instillation. After 48 hours, the animals were sacrificed and the colon was weighed, measured and scored for visible damage. Acetic acid triggered an intense inflammatory response of the colon, characterised by haemorrhage, ulceration and bowel wall thickening. From the drugs tested, only CNC (2 × 50 mg/kg) effectively depressed inflammatory damage of the colon. The mechanism of this beneficial effect remains to be elucidated.

scholarly journals Beta-Chitosane as a Treatment for Ulcerative Colitis: Therapeutic Effectiveness and Possible Mechanisms of Action

2021 ◽  
Vol 2 (3) ◽  
pp. 114-124
Author(s):  
H Laribi-Habchi ◽  
L Yasmine ◽  
S Zineb ◽  
A Boucherit ◽  
A Kenza
Keyword(s):  
Ulcerative Colitis ◽  
Acetic Acid ◽  
Histological Study ◽  
Neutrophil Infiltration ◽  
Negative Control Group ◽  
Positive Control ◽  
Negative Control ◽  
Control Group ◽  
Anti Inflammatory ◽  
Entire Treatment

Purpose: Colitis is a widespread inflammatory bowel disease with heterogeneous etiology (genetic and immunological). It is treated with drugs such as steroidal and non-steroidal anti-inflammatory that, in the long term, can cause side effects. For this reason, the exploitation of natural resources to combat this type of disease is the concern of researchers. The purpose of our study was to evaluate the anti-colitis (anti-inflammatory) effect of β-Chitosane induced in albino mice by acetic acid (5%). Methods: Mices were separated into six groups: the witness (untreated and not ulcerated), negative control group (ulcerated and untreated), the positive control ulcerated and treated with the Dexaméthasone® (1 mg/kg), and test groups ulcerated and treated with different doses of β-Chitosane (0.5 g/ kg; 0.75 g/ kg and 1 g/ kg) for the entire treatment estimated to six-days. β-Chitosane efficacy was evaluated by macroscopic and microscopic scores. Results: The clinical scores showed that β-Chitosane with a dose of 1 g/kg for the entire treatment significantly reduced the damage caused by acetic acid with a score of (3.41 ± 1.45) compared to those of the positive control which reduced less the inflammation (6.26 ± 1.23). The histological study of the colons was able to validate the effect of β-Chitosane by decreasing neutrophil infiltration and ulceration in the colon as well as by structural recovery of the mucosa. Conclusion: These results provide evidence that β-Chitosane has a protective effect against ulcerative colitis that may be due to its antioxidant, anti infectious, anti-inflammatory and healing activities.

scholarly journals Dietary Curcumin Alleviated Aflatoxin B1-Induced Acute Liver Damage in Ducks by Regulating NLRP3–Caspase-1 Signaling Pathways

Foods ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3086
Author(s):  
Sanjun Jin ◽  
Hao Yang ◽  
Yingjie Wang ◽  
Qian Pang ◽  
Yihan Jiao ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Dna Adducts ◽  
Liver Damage ◽  
Aflatoxin B1 ◽  
Control Group ◽  
Oxidation Stress ◽  
Basic Diet ◽  
Caspase 1

Aflatoxin B1 (AFB1) is a mycotoxin widely distributed in animal feed and human food; it represents a serious threat to human and animal health. This study investigates the mechanism by which dietary curcumin protected liver against acute damage caused by AFB1 administration in ducks. One-day-old male ducks (n = 450) were randomly assigned to three groups, the control group, the AFB1 group, and the AFB1 + curcumin group; the first group were fed with basic diet, while the third group was fed basic diet containing 500 mg/kg curcumin. Ducks in the AFB1 group and AFB1 + curcumin group were challenged with AFB1 at the age of 70 days. The results show that AFB1 administration caused liver damage, increased CYP450 content and AFB1-DNA adducts in the liver, and induced oxidative stress and inflammatory response in the liver. Dietary curcumin significantly inhibited the generation of H2O2 and MDA in liver, activated the Nrf2-ARE signaling pathway, and suppressed the NLRP3–caspase-1 signaling pathway in the liver of ducks. Conclusively, curcumin in diet could protect duck liver against the generation of AFB1-DNA adducts, toxicity, oxidation stress and inflammatory response induced by AFB1 through regulating the NLRP3–caspase-1 signaling pathways, demonstrating that curcumin is a potential feed additive agent to reduce the serious harmful effects of AFB1 on duck breeding.

scholarly journals EVALUATION OF ANTIHYPERLIPIDEMIC, ANTI-INFLAMMATORY, AND ANALGESIC ACTIVITIES OF EURYCOMA LONGIFOLIA IN ANIMAL MODELS

2017 ◽  
Vol 9 (3) ◽  
pp. 166
Author(s):  
Phebe Hendra ◽  
Fenty . ◽  
Putu Ririn Andreani ◽  
Bernadetha Maria Estika Pangestuti ◽  
Jeffry Julianus
Keyword(s):  
Acetic Acid ◽  
Control Group ◽  
Root Extract ◽  
Paw Edema ◽  
Edema Formation ◽  
Eurycoma Longifolia ◽  
Anti Inflammatory ◽  
Analgesic Activities ◽  
Enrich Diet ◽  
Digital Caliper

Objective: To investigate the antihyperlipidemic, anti-inflammatory and analgesic properties of of E. longifolia root extract in animal models.Methods: In this study, glucose-fructose enriched diet-induced hyperlipidemia, carrageenan-induced paw edema and acetic acid-induced writhing were used to evaluate the anti-hypertriglyceridemia, anti-inflammatory and analgesic activities, respectively. At the end of the experiment of glucose-fructose enriched diet-induced hyperlipidemia, blood samples were collected and estimation of blood lipids were carried out. Edema thickness was measured using digital caliper at 0, 15, 30, 45, 60, 90, 120, 150, 180, 210, 240, 270, 300, 330, and 360 min after carrageenan injection. The number of abdominal writhing for each mouse was observed and counted during a period of 1 h post injection of acetic acid.Results: E. longifolia root extract demonstrated a significant reduction of triglyceride levels (p<0.05) compared with the control group in glucose-fructose enrich diet in rats. In anti-inflammatory test, the extract significantly inhibited the carrageenan induced paw edema formation (p<0.05). The extract also significantly decreased the number of writhing in acetic acid-induced mice (p<0.05).Conclusion: E. longifolia root extract shown a significant anti-hypertriglyceridemia, anti-inflammatory and analgesic activities. Further studies are needed to determine mechanisms for its acitivities of E. longifolia root extract.

Diphenyl diselenide subcutaneous supplementation of dairy sheep: effects on oxidant and antioxidant status, inflammatory response and milk composition

2019 ◽  
Vol 59 (3) ◽  
pp. 461 ◽  
Author(s):  
Angelisa H. Biazus ◽  
Chrystian J. Cazarotto ◽  
Gustavo Machado ◽  
Nathieli B. Bottari ◽  
Mariana S. Alves ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Interleukin 10 ◽  
Milk Composition ◽  
Fat Content ◽  
Control Group ◽  
Lactation Period ◽  
Diphenyl Diselenide ◽  
Dairy Sheep ◽  
Positive Effects ◽  
Anti Inflammatory

Diphenyl diselenide ((PhSe)2) is a organoselenium compound with potent antioxidant properties. Therefore, the aim of the present study was to evaluate whether subcutaneous supplementation of (PhSe)2 in dairy sheep has positive effects on milk composition, as well as on the prevention of oxidative stress and exacerbated inflammatory response. For this, 16 primiparous recently calved sheep were divided into the following two groups, with eight animals in each: Group A, the control group; and Group B, the group subcutaneously supplemented with five doses of (PhSe)2 of 3.0µmol/kg each every 7 days. Blood samples from supplemented animals showed increased concentration of antioxidant enzymes (catalase, superoxide dismutase, glutathione peroxidase and glutathione-S-transferase), and reduced reactive oxygen species and lipid peroxidation, which prevented oxidative damage in the lactation period, as well as increased seric interleukin-10, an anti-inflammatory cytokine. In the sera, supplemented animals showed increased total antioxidant capacity and ferric-reducing ability of plasma compared with the control group. As a consequence, supplemented animals showed increased antioxidant variables, as well as reduced protein oxidation in milk samples. Moreover, milk from supplemented sheep showed a higher fat content, and lower total protein and lactose contents in some periods in the study, than did not-supplemented ewes. Seric concentrations of interleukin-1 were lower on Days 30 and 45 in supplemented animals, as well as the concentrations of tumour necrosis factor α in all periods, than were those in the control group, whereas the interleukin-10 concentrations were higher. Thus, dairy sheep supplementation of (PhSe)2 activated antioxidant and anti-inflammatory responses, and increased milk fat content. Moreover, this protocol increased the antioxidant and, consequently, reduced the oxidant concentration in milk, which is desirable for product quality.

scholarly journals Dynamic Evaluation of Compound Ento-PB for the Repair of Mucosal Ulcer in Dogs With Acetic Acid-induced Experimental Colitis 

2020 ◽  
Author(s):  
Jin-hu Chen ◽  
Jian-ting Zhao ◽  
Zheng-yong Yu ◽  
Yi-hao Che ◽  
Yu-jia Wang ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Acetic Acid ◽  
Inflammatory Cytokines ◽  
Mucosal Healing ◽  
Dynamic Monitoring ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Expression Levels ◽  
Cox 2 ◽  
Anti Inflammatory

Abstract Background: Mucosal inflammation and ulcer play important roles in the pathogenesis of ulcerative colitis. As as traditional Chinese medicine compound composed of Periplaneta americana and Taraxacum mongolicum, Ento-PB is always prescribed for the treatment of ulcer and inflammatory diseases. As for the significant role of P. americana in terms of promoting mucosal healing, the compatibility of the anti-inflammatory drug T. mongolicum may enable Ento-PB to simultaneously play anti-inflammatory and promote mucosal healing effects on the treatment of UC. Therefore, this study aimed to evaluate the therapeutic potential and possible mechanism of Ento-PB for UC by establishing an acetic acid-induced colitis model in dogs.Methods: Preliminary identification to the chemical components of compound Ento-PB was carried out through high performance liquid chromatography. A cross-bred dogs model of acetic acid-induced ulcerative colitis was established to evaluate the efficacy of compound Ento-PB. The expression levels of inflammatory cytokines C-reactive protein (CRP), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-10 (IL-10) in plasma were measured by carrying out enzyme-linked immunosorbent assay (ELISA).Results: With the extension of treatment time, Ento-PB could effectively improve clinical symptoms of UC cross-bred dogs. Colonoscopy displayed that mucosal redness, swelling and congestion decreased gradually, and obviously repaired after mucosal injury. The intestinal texture was gradually clear, and the colonoscopy score gradually reduced. Histopathological examination revealed that the structure of colon was restored significantly, the infiltration of inflammatory cells was reduced, and the histological score was remarkably reduced. At the same time, the results of dynamic monitoring of inflammatory cytokines in plasma proved that Ento-PB can gradually down-regulate the activity of CRP, iNOS and COX-2, reduce the expression levels of inflammatory cytokines TNF-α and IL-1β, and gradually restore anti-inflammatory and the expression level of cytokine IL-10.Conclusions: Ento-PB reduces the level of pro-inflammatory cytokines in a dose- and time-dependent manner and inflammation, improves colon tissue lesions and the repair of intestinal mucosa after injury, and effectively increases acetic acid-induced colon inflammation in UC cross-bred dogs.

scholarly journals Investigation of Potential Genetic Biomarkers and Molecular Mechanism of Ulcerative Colitis Utilizing Bioinformatics Analysis

2019 ◽  
Author(s):  
Jiaqi Zhang ◽  
Xue Wang ◽  
Lin Xu ◽  
Zedan Zhang ◽  
Fengyun Wang ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Gene Therapy ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Functional Enrichment ◽  
Hub Genes ◽  
Amyloid A ◽  
Chemokine Signaling ◽  
Chemokine Signaling Pathway ◽  
Potential Biomarkers

Abstract Objectives: To reveal the molecular mechanisms of ulcerative colitis (UC) and provide potential biomarkers for UC gene therapy. Methods: We downloaded the GSE87473 microarray dataset from the Gene Expression Omnibus (GEO) and identified the differentially expressed genes (DEGs) between UC samples and normal samples. Then ,a module partition analysis was performed based on a weighted gene co-expression network analysis (WGCNA),followed by pathway and functional enrichment analyses. Furthermore, we investigated the hub genes . At last, data validation was performed to ensure the reliability of the hub genes. Results: Between UC group and normal group, 988 DEGs were investigated . The DEGs were clustered into 5 modules using WGCNA. These DEGs were mainly enriched in functions such as the immune response, the inflammatory response and chemotaxis, and they were mainly enriched in KEGG pathways such as the cytokine-cytokine receptor interaction , chemokine signaling pathway, and complement and coagulation cascades. The hub genes, including dual oxidase maturation factor 2(DUOXA2), serum amyloid A (SAA) 1 and SAA2, TNFAIP3-interacting protein 3(TNIP3), C-X-C motif chemokine (CXCL1), solute carrier family 6 member 14(SLC6A14) and complement decay-accelerating factor (CD antigen CD55),were revealed as potential tissue biomarkers for UC diagnosis or treatment. Conclusions: This study provides supportive evidence that DUOXA2, A-SAA, TNIP3, CXCL1, SLC6A14 and CD55 might be used as potential biomarkers for tissue biopsy of UC, especially SLC6A14 and CD55, which may be new targets for UC gene therapy. Moreover, the DUOX2/DUOXA2, NF-κB /TNIP3 and CXCL1/CXCR2 pathways might play an important role in the progression of UC through the chemokine signaling pathway and inflammatory response.

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