Abstract

To study the anti-inflammatory actions of electroacupuncture (EAc) on an experimental colitis model in mice. Thirty-eight male Swiss mice, divided in five groups, were subjected to induction of colitis by TNBS in 50% ethanol. Saline (SAL) and ethanol (ETNL) groups served as controls. TNBS+EAc and TNBS+ dexamethasone subgroups were treated with EAc 100Hz and dexamethasone (DEXA) 1 mg/Kg/day, respectively. After three days, a colon segment was obtained for quantification of myeloperoxidase (MPO) activity, immunohistochemistry for iNOS, malondialdehyde (MDA) and cytokines (IL-1β and IL-10). Neutrophilic activity, assayed as MPO activity, was significantly higher in the TNBS colitis group than that in the saline control group. TNBS+EAc group showed suppression of IL-10 in the colon. EAc treatment significantly reduced the concentration of MDA and the expression of iNOS, as compared to the other groups. Electroacupuncture 100Hz applied to acupoint ST-36 promotes an anti-inflammatory action on the TNBS-induced colitis, mediated by increase of IL-10 and decrease of iNOS expression.

Highlights

  • Electroacupuncture 100Hz applied to acupoint ST36 promotes an anti-inflammatory action on the TNBS-induced colitis, mediated by increase of IL-10 and decrease of iNOS expression

  • Inflammatory bowel disease (IBD) is an immune-mediated chronic intestinal condition mostly represented by ulcerative colitis and Crohn’s disease

  • Experimental colitis animal models have been developed to study the mechanisms of IBD, and are tools for pre-clinical evaluation of new treatments efficacy

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Summary

Introduction

Inflammatory bowel disease (IBD) is an immune-mediated chronic intestinal condition mostly represented by ulcerative colitis and Crohn’s disease. Both exogenous factors (e.g. composition of normal intestinal microbiota) and endogenous host factors (intestinal epithelial cell barrier function, innate and adaptive immune function) interact to cause a chronic state of dysregulated mucosal immune function. The mainstay of therapy for IBD is 5-aminosalicylic acid (5-ASA) agents and glucocorticoids as well as other immunosuppressant drugs. The long term use of such agents may give rise to adverse side effects2,3a fungal decapeptide first introduced in 1983, has significantly improved the outcome of renal transplantation, and remains the first line immunosupressant for pediatric recipients. CsA has a narrow therapeutic range because of the fine line between adequate immunosuppression and the risk of drug-induced side effects

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