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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Kolgazi, Meltem Uslu, Unal Yuksel, Meral Velioglu-Ogunc, Ayliz Ercan, Feriha Alican, Inci |
| Description | Country affiliation: Turkey Author Affiliation: Kolgazi M ( Marmara University School of Medicine, Department of Physiology, Istanbul, Turkey.) |
| Abstract | The 'cholinergic anti-inflammatory pathway' provides neurological modulation of cytokine synthesis to limit the magnitude of the immune response. This study aimed to evaluate the impact of the cholinergic anti-inflammatory pathway on the extent of tissue integrity, oxidant-antioxidant status and neutrophil infiltration to the inflamed organ in a rat model of acetic acid-induced colitis. Colitis was induced by intrarectal administration of 5% acetic acid (1ml) to Sprague-Dawley rats (200-250g; n=7-8 per group). Control group received an equal volume of saline intrarectally. The rats were treated with either nicotine (1mg/kg/day) or huperzine A (0.1mg/kg/day) intraperitoneally for 3 days. After decapitation, the distal colon was scored macroscopically and microscopically. Tissue samples were used for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, and myeloperoxidase (MPO) activity. Formation of reactive oxygen species was monitored by using chemiluminescence (CL). Nuclear factor (NF)-κB expression was evaluated in colonic samples via immunohistochemical analysis. Trunk blood was collected for the assessment of tumor necrosis factor (TNF)- , interleukin (IL)-1ß, IL-10, resistin and visfatin levels. Both nicotine and huperzine A reduced the extent of colonic lesions, increased colonic MDA level, high MPO activity and NF-κB expression in the colitis group. Elevation of serum IL-1ß level due to colitis was also attenuated by both treatments. Additionally, huperzine A was effective to reverse colitis-induced high lucigenin-enhanced CL values and serum TNF- levels. Colitis group revealed decreased serum visfatin levels compared to control group which was completely reversed by nicotine. In conclusion, modulation of the cholinergic system either by nicotine or ACh esterase inhibition improved acetic acid-induced colonic inflammation as confirmed by macroscopic and microscopic examination and biochemical assays. |
| File Format | HTM / HTML |
| ISSN | 00092797 |
| Issue Number | 1 |
| Volume Number | 205 |
| e-ISSN | 18727786 |
| Journal | Chemico-Biological Interactions |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2013-09-05 |
| Publisher Place | Ireland |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Discipline Biochemistry Discipline Pharmacology Colitis Etiology Neuroimmunomodulation Physiology Acetic Acid Toxicity Alkaloids Pharmacology Animals Antioxidants Metabolism Cholinergic Neurons Drug Effects Cholinesterase Inhibitors Immunology Physiopathology Colon Pathology Cytokines Blood Female Glutathione Male Malondialdehyde Nf-kappa B Nicotinamide Phosphoribosyltransferase Nicotine Nicotinic Agonists Peroxidase Rats Rats, Sprague-dawley Resistin Sesquiterpenes Journal Article Research Support, Non-u.s. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Medicine Toxicology |
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