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The role of cholinergic anti-inflammatory pathway in acetic acid-induced colonic inflammation in the rat

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dc.contributor.authorVELİOĞLU ÖĞÜNÇ, AYLİZ
dc.contributor.authorsKolgazi, Meltem; Uslu, Unal; Yuksel, Meral; Velioglu-Ogunc, Ayliz; Ercan, Feriha; Alican, Inci
dc.date.accessioned2022-03-12T18:09:07Z
dc.date.available2022-03-12T18:09:07Z
dc.date.issued2013
dc.description.abstractThe 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 (1 ml) to Sprague-Dawley rats (200-250 g; n = 7-8 per group). Control group received an equal volume of saline intrarectally. The rats were treated with either nicotine (1 mg/kg/day) or huperzine A (0.1 mg/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)-kappa B expression was evaluated in colonic samples via immunohistochemical analysis. Trunk blood was collected for the assessment of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, 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-kappa B expression in the colitis group. Elevation of serum IL-1 beta 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-alpha 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. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
dc.identifier.doi10.1016/j.cbi.2013.06.009
dc.identifier.eissn1872-7786
dc.identifier.issn0009-2797
dc.identifier.pubmed23810507
dc.identifier.urihttps://hdl.handle.net/11424/231241
dc.identifier.wosWOS:000331169900011
dc.language.isoeng
dc.publisherELSEVIER IRELAND LTD
dc.relation.ispartofCHEMICO-BIOLOGICAL INTERACTIONS
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectAcetic acid
dc.subjectCholinergic
dc.subjectColitis
dc.subjectHuperzine A
dc.subjectNicotine
dc.subjectRat
dc.subjectINDUCED OXIDATIVE INJURY
dc.subjectKAPPA-B ACTIVATION
dc.subjectVAGUS NERVE
dc.subjectPHEOCHROMOCYTOMA CELLS
dc.subjectRHEUMATOID-ARTHRITIS
dc.subjectEXPERIMENTAL SEPSIS
dc.subjectENHANCING FACTOR
dc.subjectGENE-EXPRESSION
dc.subjectREACTIVE OXYGEN
dc.subjectSTIMULATION
dc.titleThe role of cholinergic anti-inflammatory pathway in acetic acid-induced colonic inflammation in the rat
dc.typearticle
dspace.entity.typePublication
local.avesis.id55db345f-1b09-4240-aa31-96de978fd16e
local.import.packageSS17
local.indexed.atWOS
local.indexed.atSCOPUS
local.indexed.atPUBMED
local.journal.numberofpages9
oaire.citation.endPage80
oaire.citation.issue1
oaire.citation.startPage72
oaire.citation.titleCHEMICO-BIOLOGICAL INTERACTIONS
oaire.citation.volume205
relation.isAuthorOfPublication13300bf6-ba96-4f87-9868-b0d2c86f572a
relation.isAuthorOfPublication.latestForDiscovery13300bf6-ba96-4f87-9868-b0d2c86f572a

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