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

摘要: The "cholinergic anti-inflammatory pathway" provides neurological modulation of cytokine synthesis to limit the magnitude immune response. This study aimed evaluate impact cholinergic pathway on extent tissue integrity, oxidant-antioxidant status and neutrophil infiltration inflamed organ in a rat model acetic acid-induced colitis. Colitis was induced by intrarectal administration 5% acid (1ml) Sprague-Dawley rats (200-250g; n=7-8 per group). Control group received an equal volume saline intrarectally. were treated with either nicotine (1mg/kg/day) or huperzine A (0.1mg/kg/day) intraperitoneally for 3 days. After decapitation, distal colon scored macroscopically microscopically. Tissue samples used measurement malondialdehyde (MDA) glutathione (GSH) levels, myeloperoxidase (MPO) activity. Formation reactive oxygen species monitored using chemiluminescence (CL). Nuclear factor (NF)-κB expression evaluated colonic via immunohistochemical analysis. Trunk blood collected assessment tumor necrosis (TNF)-α, interleukin (IL)-1β, IL-10, resistin visfatin levels. Both reduced lesions, increased MDA level, high MPO activity NF-κB colitis group. Elevation serum IL-1β level due also attenuated both treatments. Additionally, effective reverse colitis-induced lucigenin-enhanced CL values TNF-α revealed decreased levels compared control which completely reversed nicotine. In conclusion, system ACh esterase inhibition improved inflammation as confirmed macroscopic microscopic examination biochemical assays.