Molecular evidences on the benefit of N-acetylcysteine in experimental colitis

AbstractInflammatory bowel disease (IBD) is a chronic recurrent disease of the digestive tract with an unknown etiology. The aim of this study was to examine the possible protective effects of N-acetylcysteine (NAC) in the mouse model of IBD by measuring specific biomarkers in the colon cells. Colitis was induced by administration of dextran sodium sulfate (DSS) in drinking water (3%) for 7 days. Three doses of NAC (106, 160, and 240 mg/kg) were given after induction of colitis (4 days post DSS) for 4 days by gavage. Lipid peroxides (LP), total antioxidant power (TAP), total thiol molecules (TTM), tumor necrosis factor-α (TNF-α), nitric oxide (NO), superoxide dismutase (SOD), and catalase (CAT) were measured in the colon homogenate of the treated animals. NAC (160 and 240 mg/kg) significantly decreased LP, TNF-α, NO and increased TTM, SOD, and CAT. The TAP was also increased by NAC (240 mg/kg). It is concluded that moderate to high doses of NAC improves cellular biomarkers of IBD in mice. Further studies should be trialled in humans suffering from two common inflammatory bowel disease called ulcerative colitis and Crohn’s disease.

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Protective effects of bioactive peptides in foxtail millet protein hydrolysates against experimental colitis in mice

Food & Function ◽

10.1039/d1fo02482e ◽

2022 ◽

Author(s):

Bowei Zhang ◽

Yingchuan Xu ◽

Congying Zhao ◽

Yunhui Zhang ◽

Huan Lv ◽

...

Keyword(s):

Inflammatory Bowel Disease ◽

Bowel Disease ◽

Bioactive Peptides ◽

Dietary Intervention ◽

Foxtail Millet ◽

Intervention Strategy ◽

Experimental Colitis ◽

Protective Effects ◽

Active Ingredients ◽

Inflammatory Bowel

It is of great significance to develop a dietary intervention strategy to prevent inflammatory bowel disease (IBD). A millet-rich diet can ameliorate IBD, but the active ingredients and mechanisms remain...

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Cytokines in canine inflammatory bowel disease

Polish Journal of Veterinary Sciences ◽

10.2478/pjvs-2013-0025 ◽

2013 ◽

Vol 16 (1) ◽

pp. 165-171 ◽

Cited By ~ 13

Author(s):

A. Kołodziejska-Sawerska ◽

A. Rychlik ◽

A. Depta ◽

M. Wdowiak ◽

M. Nowicki ◽

...

Keyword(s):

Inflammatory Bowel Disease ◽

Mrna Expression ◽

Lamina Propria ◽

Bowel Disease ◽

Unknown Etiology ◽

Tnf Α ◽

Chronic Enteropathies ◽

Inflammatory Bowel ◽

Ifn Γ

Abstract Canine inflammatory bowel disease is a group of chronic enteropathies characterized by persistent or recurring gastric symptoms with an unknown etiology which are related to histopathological changes in the mucosa of the small and large bowel in the form of cellular infiltration in the mucosal lamina propria. Recent years have witnessed a growing number of investigations into the role of the immune system and, in particular, cytokines in the development of IBD. In this article, the expression of pro-inflammatory (IL-1, IL-2, IL-5, IL-6, IL-12, IL-18, IFN-γ, TNF-α) and anti-inflammatory cytokines (IL-4, IL-10) was compared in canine patients with IBD based on clinical presentation, breed, lamina propria cell infiltrate and histopathological grade. Only selected studies confirmed higher mRNA expression levels of cytokines IL-2, IL-4, IL-5, IL-12p40, IFN-γ, TNF-α and TGF-β in dogs with IBD in comparison with healthy subjects. GSD were strongly represented in most study populations. Dogs with LPE were characterized by elevated levels of IL-1α, IL-1β, IL-2, IL-5, IL-6, IL-12, TNF-α, TGF-β. The present studies of canine patients with LPC revealed the mRNA expression of cytokines IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12p35, IL-12p40, IFN-γ, TNF-α, TGF-β. In the reviewed studies, the progression of IBD was not accompanied by changes in the mRNA expression of IL-1α, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12, IL-18, TNF-α, IFN-γ or TGF-β.

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Uhrf1-Mediated Tnf-α Gene Methylation Controls Proinflammatory Macrophages in Experimental Colitis Resembling Inflammatory Bowel Disease

The Journal of Immunology ◽

10.4049/jimmunol.1900467 ◽

2019 ◽

Vol 203 (11) ◽

pp. 3045-3053 ◽

Cited By ~ 3

Author(s):

Shanshan Qi ◽

Yongkui Li ◽

Zheng Dai ◽

Mengxi Xiang ◽

Guobin Wang ◽

...

Keyword(s):

Inflammatory Bowel Disease ◽

Bowel Disease ◽

Experimental Colitis ◽

Gene Methylation ◽

Tnf Α ◽

Inflammatory Bowel

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Cutaneous Manifestations in Biological-Treated Inflammatory Bowel Disease Patients: A Narrative Review

Journal of Clinical Medicine ◽

10.3390/jcm10051040 ◽

2021 ◽

Vol 10 (5) ◽

pp. 1040

Author(s):

Jo L. W. Lambert ◽

Sofie De Schepper ◽

Reinhart Speeckaert

Keyword(s):

Inflammatory Bowel Disease ◽

Bowel Disease ◽

Cutaneous Manifestations ◽

Cutaneous Infections ◽

Tnf Α ◽

Common Skin ◽

Receptor Blockers ◽

Infusion Reactions ◽

Inflammatory Bowel ◽

Lichenoid Reactions

The biologic era has greatly improved the treatment of Crohn’s disease and ulcerative colitis. Biologics can however induce a wide variety of skin eruptions, especially those targeting the TNF-α and Th17 pathway. These include infusion reactions, eczema, psoriasis, lupus, alopecia areata, vitiligo, lichenoid reactions, granulomatous disorders, vasculitis, skin cancer, and cutaneous infections. It is important to recognize these conditions as treatment-induced adverse reactions and adapt the treatment strategy accordingly. Some conditions can be treated topically while others require cessation or switch of the biological therapy. TNF-α antagonists have the highest rate adverse skin eruptions followed by ustekinumab and anti-integrin receptor blockers. In this review, we provide an overview of the most common skin eruptions which can be encountered in clinical practice when treating IBD (Inflammatory bowel disease) patients and propose a therapeutic approach for each condition.

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Myeloproliferative disorders in patients with inflammatory bowel disease on anti-TNF-α therapy

Inflammatory Bowel Diseases ◽

10.1002/ibd.21291 ◽

2011 ◽

Vol 17 (2) ◽

pp. 674-675 ◽

Cited By ~ 2

Author(s):

Monika Fischer ◽

Debra J. Helper ◽

Michael V. Chiorean

Keyword(s):

Inflammatory Bowel Disease ◽

Bowel Disease ◽

Myeloproliferative Disorders ◽

Tnf Α ◽

Inflammatory Bowel

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Evaluation of Effect CAT -262C/T, SOD + 35A/C, GPx1 Pro197Leu Polymorphisms in Patients with IBD in the Polish Population

Polish Journal of Surgery ◽

10.1515/pjs-2016-0071 ◽

2016 ◽

Vol 88 (6) ◽

Cited By ~ 4

Author(s):

Jerzy Mrowicki ◽

Małgorzata Mrowicka ◽

Ireneusz Majsterek ◽

Michał Mik ◽

Adam Dziki ◽

...

Keyword(s):

Oxidative Stress ◽

Ulcerative Colitis ◽

Inflammatory Bowel Disease ◽

Antioxidant Enzymes ◽

Bowel Disease ◽

Protective Effects ◽

Polish Population ◽

Nucleotide Polymorphisms ◽

Inflammatory Bowel ◽

Genotype C

AbstractInflammatory bowel disease (IBD) are a heterogeneous group of disorders in the course dominated by chronic, recurrent gastrointestinal inflammation. It is believed that the activation of IBD occurs in patients with a genetic predisposition to their development. Chronic inflammation develops as a result of an excessive reaction of the immune system principally under the influence of environmental risk factors. Among them, it has been shown that the mechanism of oxidative stress is associated with the pathophysiology of inflammatory bowel disease, responsible for the commencement and progress of these diseases.was the relationship between single nucleotide polymorphisms (SNPs) of individual antioxidant enzymes, and the prevalence of inflammatory bowel disease that may be associated with increased levels of oxidative stress.A total of 111 IBD patients, including 65 patients with ulcerative colitis (UC) and 46 with Crohn’s disease (CD) and 125 healthy controls recruited from the Polish population, were genotyped forThe performed analysis of genetic polymorphisms of antioxidant enzymes showed that polymorphic variant of the CAT -262 C / T may have protective effects in patients with ulcerative colitis in the range of genotype C / T; OR = 0.49 (0.25-0.99), p = 0.044. Trend protective, but statistically unrelated, it was also observed for genotype T / T and T allele of the same polymorphism and genotypes and allelesIt has been shown that the polymorphism of antioxidant enzymes

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Inflammatory bowel disease: the role of inflammatory cytokine gene polymorphisms

Mediators of Inflammation ◽

10.1080/09511920410001713529 ◽

2004 ◽

Vol 13 (3) ◽

pp. 181-187 ◽

Cited By ~ 45

Author(s):

Joanna Balding ◽

Wendy J. Livingstone ◽

Judith Conroy ◽

Lesley Mynett-Johnson ◽

Donald G. Weir ◽

...

Keyword(s):

Ulcerative Colitis ◽

Inflammatory Bowel Disease ◽

Bowel Disease ◽

Disease Incidence ◽

Strong Association ◽

Tnf Α ◽

Genes Encoding ◽

Inflammatory Processes ◽

Inflammatory Bowel ◽

Cytokine Gene Polymorphisms

THE mechanisms responsible for development of inflammatory bowel disease (IBD) have not been fully elucidated, although the main cause of disease pathology is attributed to up-regulated inflammatory processes. The aim of this study was to investigate frequencies of polymorphisms in genes encoding pro-inflammatory and anti-inflammatory markers in IBD patients and controls. We determined genotypes of patients with IBD (n=172) and healthy controls (n=389) for polymorphisms in genes encoding various cytokines (interleukin (IL)-1β, IL-6, tumour necrosis factor (TNF), IL-10, IL-1 receptor antagonist). Association of these genotypes to disease incidence and pathophysiology was investigated. No strong association was found with occurrence of IBD. Variation was observed between the ulcerative colitis study group and the control population for the TNF-α-308 polymorphism (p=0.0135). There was also variation in the frequency of IL-6-174 and TNF-α-308 genotypes in the ulcerative colitis group compared with the Crohn's disease group (p=0.01). We concluded that polymorphisms in inflammatory genes are associated with variations in IBD phenotype and disease susceptibility. Whether the polymorphisms are directly involved in regulating cytokine production, and consequently pathophysiology of IBD, or serve merely as markers in linkage disequilibrium with susceptibility genes remains unclear.

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