role of cholinergic anti-inflammatory pathway in acetic acid-induced colonic inflammation in the rat
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 neu...
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| Veröffentlicht in: | Chemico-biological interactions 2013-09, Vol.205 (1), p.72-80 |
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| creator | Kolgazi, Meltem Uslu, Unal Yuksel, Meral Velioglu-Ogunc, Ayliz Ercan, Feriha Alican, Inci |
| description | 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 3days. 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)-α, interleukin (IL)-1β, 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-1β 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-α 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. |
| doi_str_mv | 10.1016/j.cbi.2013.06.009 |
| format | Article |
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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 3days. 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)-α, interleukin (IL)-1β, 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-1β 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-α 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.</description><identifier>ISSN: 0009-2797</identifier><identifier>EISSN: 1872-7786</identifier><identifier>DOI: 10.1016/j.cbi.2013.06.009</identifier><identifier>PMID: 23810507</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>acetic acid ; Acetic Acid - toxicity ; Alkaloids - pharmacology ; animal models ; Animals ; Antioxidants - metabolism ; blood serum ; chemiluminescence ; Cholinergic Neurons - drug effects ; Cholinergic Neurons - physiology ; Cholinesterase Inhibitors - pharmacology ; colitis ; Colitis - etiology ; Colitis - immunology ; Colitis - physiopathology ; colon ; Colon - drug effects ; Colon - metabolism ; Colon - pathology ; Cytokines - blood ; decapitation ; Female ; glutathione ; Glutathione - metabolism ; immune response ; immunohistochemistry ; inflammation ; interleukin-10 ; interleukin-1beta ; Male ; malondialdehyde ; Malondialdehyde - metabolism ; myeloperoxidase ; Neuroimmunomodulation - drug effects ; Neuroimmunomodulation - physiology ; NF-kappa B - metabolism ; nicotinamide phosphoribosyltransferase ; Nicotinamide Phosphoribosyltransferase - blood ; nicotine ; Nicotine - pharmacology ; Nicotinic Agonists - pharmacology ; Peroxidase - metabolism ; Rats ; Rats, Sprague-Dawley ; reactive oxygen species ; resistin ; Resistin - blood ; Sesquiterpenes - pharmacology ; transcription factor NF-kappa B ; tumor necrosis factor-alpha</subject><ispartof>Chemico-biological interactions, 2013-09, Vol.205 (1), p.72-80</ispartof><rights>Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c391t-558e4b6f2bd505bb0e937e83128109a57944d393fc54178b7996e940b349a9e53</citedby><cites>FETCH-LOGICAL-c391t-558e4b6f2bd505bb0e937e83128109a57944d393fc54178b7996e940b349a9e53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23810507$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kolgazi, Meltem</creatorcontrib><creatorcontrib>Uslu, Unal</creatorcontrib><creatorcontrib>Yuksel, Meral</creatorcontrib><creatorcontrib>Velioglu-Ogunc, Ayliz</creatorcontrib><creatorcontrib>Ercan, Feriha</creatorcontrib><creatorcontrib>Alican, Inci</creatorcontrib><title>role of cholinergic anti-inflammatory pathway in acetic acid-induced colonic inflammation in the rat</title><title>Chemico-biological interactions</title><addtitle>Chem Biol Interact</addtitle><description>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 3days. 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)-α, interleukin (IL)-1β, 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-1β 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-α 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.</description><subject>acetic acid</subject><subject>Acetic Acid - toxicity</subject><subject>Alkaloids - pharmacology</subject><subject>animal models</subject><subject>Animals</subject><subject>Antioxidants - metabolism</subject><subject>blood serum</subject><subject>chemiluminescence</subject><subject>Cholinergic Neurons - drug effects</subject><subject>Cholinergic Neurons - physiology</subject><subject>Cholinesterase Inhibitors - pharmacology</subject><subject>colitis</subject><subject>Colitis - etiology</subject><subject>Colitis - immunology</subject><subject>Colitis - physiopathology</subject><subject>colon</subject><subject>Colon - drug effects</subject><subject>Colon - metabolism</subject><subject>Colon - pathology</subject><subject>Cytokines - blood</subject><subject>decapitation</subject><subject>Female</subject><subject>glutathione</subject><subject>Glutathione - metabolism</subject><subject>immune response</subject><subject>immunohistochemistry</subject><subject>inflammation</subject><subject>interleukin-10</subject><subject>interleukin-1beta</subject><subject>Male</subject><subject>malondialdehyde</subject><subject>Malondialdehyde - metabolism</subject><subject>myeloperoxidase</subject><subject>Neuroimmunomodulation - drug effects</subject><subject>Neuroimmunomodulation - physiology</subject><subject>NF-kappa B - metabolism</subject><subject>nicotinamide phosphoribosyltransferase</subject><subject>Nicotinamide Phosphoribosyltransferase - blood</subject><subject>nicotine</subject><subject>Nicotine - pharmacology</subject><subject>Nicotinic Agonists - pharmacology</subject><subject>Peroxidase - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>reactive oxygen species</subject><subject>resistin</subject><subject>Resistin - blood</subject><subject>Sesquiterpenes - pharmacology</subject><subject>transcription factor NF-kappa B</subject><subject>tumor necrosis factor-alpha</subject><issn>0009-2797</issn><issn>1872-7786</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kF1PwyAUhonRuDn9Ad4ol960QoFSLo3xK1nihe6aUEo3lrZMoDH799Js7urknDzvm5MHgFuMcoxw-bjNdW3zAmGSozJHSJyBOa54kXFeledgjtIpK7jgM3AVwjatqKDoEswKUmHEEJ-DxrvOQNdCvXGdHYxfWw3VEG1mh7ZTfa-i83u4U3Hzq_bQDlBpEydG2yYxzahNA7Xr3JCOp4x1w8TGjYFexWtw0aoumJvjXIDV68v383u2_Hz7eH5aZpoIHDPGKkPrsi3qhiFW18gIwk1FcJG-FYpxQWlDBGk1o5hXNReiNIKimlChhGFkAR4OvTvvfkYTouxt0Kbr1GDcGCSmyVVJKa4Sig-o9i4Eb1q587ZXfi8xkpNcuZVJrpzkSlTKZDJl7o71Y92b5pT4t5mA-wPQKifV2tsgV1-pgSXxZcXT63-QMX8L</recordid><startdate>20130905</startdate><enddate>20130905</enddate><creator>Kolgazi, Meltem</creator><creator>Uslu, Unal</creator><creator>Yuksel, Meral</creator><creator>Velioglu-Ogunc, Ayliz</creator><creator>Ercan, Feriha</creator><creator>Alican, Inci</creator><general>Elsevier Ireland Ltd</general><scope>FBQ</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20130905</creationdate><title>role of cholinergic anti-inflammatory pathway in acetic acid-induced colonic inflammation in the rat</title><author>Kolgazi, Meltem ; Uslu, Unal ; Yuksel, Meral ; Velioglu-Ogunc, Ayliz ; Ercan, Feriha ; Alican, Inci</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c391t-558e4b6f2bd505bb0e937e83128109a57944d393fc54178b7996e940b349a9e53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>acetic acid</topic><topic>Acetic Acid - toxicity</topic><topic>Alkaloids - pharmacology</topic><topic>animal models</topic><topic>Animals</topic><topic>Antioxidants - metabolism</topic><topic>blood serum</topic><topic>chemiluminescence</topic><topic>Cholinergic Neurons - drug effects</topic><topic>Cholinergic Neurons - physiology</topic><topic>Cholinesterase Inhibitors - pharmacology</topic><topic>colitis</topic><topic>Colitis - etiology</topic><topic>Colitis - immunology</topic><topic>Colitis - physiopathology</topic><topic>colon</topic><topic>Colon - drug effects</topic><topic>Colon - metabolism</topic><topic>Colon - pathology</topic><topic>Cytokines - blood</topic><topic>decapitation</topic><topic>Female</topic><topic>glutathione</topic><topic>Glutathione - metabolism</topic><topic>immune response</topic><topic>immunohistochemistry</topic><topic>inflammation</topic><topic>interleukin-10</topic><topic>interleukin-1beta</topic><topic>Male</topic><topic>malondialdehyde</topic><topic>Malondialdehyde - metabolism</topic><topic>myeloperoxidase</topic><topic>Neuroimmunomodulation - drug effects</topic><topic>Neuroimmunomodulation - physiology</topic><topic>NF-kappa B - metabolism</topic><topic>nicotinamide phosphoribosyltransferase</topic><topic>Nicotinamide Phosphoribosyltransferase - blood</topic><topic>nicotine</topic><topic>Nicotine - pharmacology</topic><topic>Nicotinic Agonists - pharmacology</topic><topic>Peroxidase - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>reactive oxygen species</topic><topic>resistin</topic><topic>Resistin - blood</topic><topic>Sesquiterpenes - pharmacology</topic><topic>transcription factor NF-kappa B</topic><topic>tumor necrosis factor-alpha</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kolgazi, Meltem</creatorcontrib><creatorcontrib>Uslu, Unal</creatorcontrib><creatorcontrib>Yuksel, Meral</creatorcontrib><creatorcontrib>Velioglu-Ogunc, Ayliz</creatorcontrib><creatorcontrib>Ercan, Feriha</creatorcontrib><creatorcontrib>Alican, Inci</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Chemico-biological interactions</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kolgazi, Meltem</au><au>Uslu, Unal</au><au>Yuksel, Meral</au><au>Velioglu-Ogunc, Ayliz</au><au>Ercan, Feriha</au><au>Alican, Inci</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>role of cholinergic anti-inflammatory pathway in acetic acid-induced colonic inflammation in the rat</atitle><jtitle>Chemico-biological interactions</jtitle><addtitle>Chem Biol Interact</addtitle><date>2013-09-05</date><risdate>2013</risdate><volume>205</volume><issue>1</issue><spage>72</spage><epage>80</epage><pages>72-80</pages><issn>0009-2797</issn><eissn>1872-7786</eissn><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 3days. 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)-α, interleukin (IL)-1β, 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-1β 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-α 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.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>23810507</pmid><doi>10.1016/j.cbi.2013.06.009</doi><tpages>9</tpages></addata></record> |
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| subjects | acetic acid Acetic Acid - toxicity Alkaloids - pharmacology animal models Animals Antioxidants - metabolism blood serum chemiluminescence Cholinergic Neurons - drug effects Cholinergic Neurons - physiology Cholinesterase Inhibitors - pharmacology colitis Colitis - etiology Colitis - immunology Colitis - physiopathology colon Colon - drug effects Colon - metabolism Colon - pathology Cytokines - blood decapitation Female glutathione Glutathione - metabolism immune response immunohistochemistry inflammation interleukin-10 interleukin-1beta Male malondialdehyde Malondialdehyde - metabolism myeloperoxidase Neuroimmunomodulation - drug effects Neuroimmunomodulation - physiology NF-kappa B - metabolism nicotinamide phosphoribosyltransferase Nicotinamide Phosphoribosyltransferase - blood nicotine Nicotine - pharmacology Nicotinic Agonists - pharmacology Peroxidase - metabolism Rats Rats, Sprague-Dawley reactive oxygen species resistin Resistin - blood Sesquiterpenes - pharmacology transcription factor NF-kappa B tumor necrosis factor-alpha |
| title | role of cholinergic anti-inflammatory pathway in acetic acid-induced colonic inflammation in the rat |
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