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ToxSci Advance Access published online on June 23, 2005
Toxicological Sciences, doi:10.1093/toxsci/kfi238
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© The Author 2005. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
Received April 12, 2005
Accepted June 1, 2005

Systems Toxicology

The Diverse Actions of Nicotine and Different Extracted Fractions from Tobacco Smoke Against Hapten-Induced Colitis in Rats

Joshua K.S. Ko 1* and Chi-Hin Cho 2

1 School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China
2 Department of Pharmacology, Faculty of Medicine, The University of Hong Kong, Hong Kong, China

* To whom correspondence should be addressed.
Joshua K.S. Ko, E-mail: jksko{at}hkbu.edu.hk


  Abstract

The etiology of ulcerative colitis (UC) remains unknown, while the risk of developing UC is apparently higher in non-smokers and ex-smokers. We have demonstrated in a colitis animal model that exposure to tobacco smoke could attenuate UC pathogenesis. The present study aimed to investigate and compare between the modes of action of nicotine and different fractions of tobacco smoke extract in the development of experimental colitis. The hapten 2,4-dinitrobenzene sulphonic acid (DNBS) was used to induce colitis in Sprague-Dawley rats. Results indicated that both tobacco smoke exposure and subcutaneous nicotine differentially reduced colonic lesion size, myeloperoxidase (MPO) activity, luminolamplified free radicals generation and leukotriene B4 formation in the inflamed colon of colitis animals. These phenomena were accompanied by the down-regulation of colonic interleukin (IL)-1{beta} and monocyte chemoattractant protein (MCP)-1 protein expression. By treating the colitic animals with various tobacco extracts, we further discovered that ethanol extract from filtered tobacco smoke could attenuate DNBS-evoked colonic damage and the elevated MPO activity, while at the same time down-regulated colonic IL-1{beta} and MCP-1 protein expression. On the contrary, the highest dose of the chloroform extract from the cigarette filter caused aggravating effects and overexpression of the pro-inflammatory cytokines and chemokines. These data suggest that effective attenuation of DNBS-induced colitis by tobacco smoke could be due to its nicotine content and possibly other flavonoid components that are found in the ethanol smoke extract.

Keywords: nicotine; tobacco smoke; neutrophils; chemotactic factors; colitis.
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