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Review article: the role of oxidative stress in pathogenesis and treatment of inflammatory bowel diseases.

作者信息

Piechota-Polanczyk Aleksandra, Fichna Jakub

机构信息

Department of Biochemistry, Faculty of Medicine, Medical University of Lodz, Mazowiecka 6/8, 92-215, Lodz, Poland.

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 2014 Jul;387(7):605-20. doi: 10.1007/s00210-014-0985-1. Epub 2014 May 6.


DOI:10.1007/s00210-014-0985-1
PMID:24798211
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4065336/
Abstract

In this review, we focus on the role of oxidative stress in the aetiology of inflammatory bowel diseases (IBD) and colitis-associated colorectal cancer and discuss free radicals and free radical-stimulated pathways as pharmacological targets for anti-IBD drugs. We also suggest novel anti-oxidative agents, which may become effective and less-toxic alternatives in IBD and colitis-associated colorectal cancer treatment. A Medline search was performed to identify relevant bibliography using search terms including: 'free radicals,' 'antioxidants,' 'oxidative stress,' 'colon cancer,' 'ulcerative colitis,' 'Crohn's disease,' 'inflammatory bowel disease.' Several therapeutics commonly used in IBD treatment, among which are immunosuppressants, corticosteroids and anti-TNF-α antibodies, could also affect the IBD progression by interfering with cellular oxidative stress and cytokine production. Experimental data shows that these drugs may effectively scavenge free radicals, increase anti-oxidative capacity of cells, influence multiple signalling pathways, e.g. MAPK and NF-kB, and inhibit pro-oxidative enzyme and cytokine concentration. However, their anti-oxidative and anti-inflammatory effectiveness still needs further investigation. A highly specific antioxidative activity may be important for the clinical treatment and relapse of IBD. In the future, a combination of currently used pharmaceutics, together with natural and synthetic anti-oxidative compounds, like lipoic acid or curcumine, could be taken into account in the design of novel anti-IBD therapies.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9f6/4065336/5303b45edd8b/210_2014_985_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9f6/4065336/6ca1e20f7663/210_2014_985_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9f6/4065336/5303b45edd8b/210_2014_985_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9f6/4065336/6ca1e20f7663/210_2014_985_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9f6/4065336/5303b45edd8b/210_2014_985_Fig2_HTML.jpg

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[1]
Review article: the role of oxidative stress in pathogenesis and treatment of inflammatory bowel diseases.

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[1]
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Naunyn Schmiedebergs Arch Pharmacol. 2025-9-5

[2]
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[3]
A bibliometric study of the most-cited research articles and reviews in Naunyn-Schmiedeberg's Archives of Pharmacology (1969-2024).

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[4]
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[6]
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[7]
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[8]
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[9]
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[10]
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本文引用的文献

[1]
Patterns of colorectal cancer care in Europe, Australia, and New Zealand.

J Natl Cancer Inst Monogr. 2013

[2]
Protection against peroxynitrite-induced DNA damage by mesalamine: implications for anti-inflammation and anti-cancer activity.

Mol Cell Biochem. 2013-3-26

[3]
IL-23/IL-17A axis correlates with the nitric oxide pathway in inflammatory bowel disease: immunomodulatory effect of retinoic acid.

J Interferon Cytokine Res. 2013-3-8

[4]
Immunohistochemical study of the Nrf2 pathway in colorectal cancer: Nrf2 expression is closely correlated to Keap1 in the tumor and Bach1 in the normal tissue.

Appl Immunohistochem Mol Morphol. 2013-12

[5]
Novel effects of ectoine, a bacteria-derived natural tetrahydropyrimidine, in experimental colitis.

Phytomedicine. 2013-2-28

[6]
Catalase gene C-262T polymorphism: importance in ulcerative colitis.

J Gastroenterol Hepatol. 2013-5

[7]
Lactulose mediates suppression of dextran sodium sulfate-induced colon inflammation by increasing hydrogen production.

Dig Dis Sci. 2013-1-31

[8]
Role of N-acetylcysteine and GSH redox system on total and active MMP-2 in intestinal myofibroblasts of Crohn's disease patients.

Int J Colorectal Dis. 2012-12-28

[9]
Reactive oxygen species mediate Cr(VI)-induced S phase arrest through p53 in human colon cancer cells.

J Environ Pathol Toxicol Oncol. 2012

[10]
Glutathione transporters.

Biochim Biophys Acta. 2013-5

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