Anticolitis Activity of Myrobalan Powder via Regulating Colonic Enterochromaffin Cells and Serotonin

Download Article

DOI: 10.21522/TIJAR.2014.03.02.Art013

Authors : Shirish Sharma, Sanjay Vaze, Harish Kumar Lalan

Abstract:

Objective: To investigate whether Myrobalan powder has an anti-inflammatory effect on colonic inflammation and to explore the mechanism involved.

Materials and Methods: Myrobalan powder was orally administrated to trinitrobenzene sulfonic acid (TNBS)-induced colitis mice at the dose of 3, 6, and 12 g/kg/d for 7 consecutive days. Body weight, stool consistency, histopathological score, and myeloperoxidase (MPO) activity were tested to evaluate the effect of Myrobalan powder on colonic inflammation while colonic enterochromaffin (EC) cell density and serotonin 5-hydroxytryptamine (5-HT) content were investigated to identify the effect of Myrobalan powder on colonic 5-HT availability.

Results: The results showed that the body weight of colitis mice was markedly decreased by 10, 12, 14, and 17% at 1, 3, 5, and 7 days (P< 0.05), whereas stool consistency score (3.6 vs. 0.4, P< 0.05), histopathological score (3.6 vs. 0.3, P< 0.05), and MPO activity (2.7 vs. 0.1,P< 0.05) in colitis mice were significantly increased compared to that of the normal mice; Myrobalan powder treatment dose-dependently increased the body weight (7–13% increase) and decreased the stool consistency score (0.4–1.4 decrease), histopathological score (0.2–0.7 decrease), and MPO activity (0.1–0.9 decrease) in colitis mice. Colonic EC cell density (70% increase) and 5-HT content (40% increase) were markedly increased in colitis mice (P< 0.05), Myrobalan powder treatment dose-dependently reduced EC cell density (20–50% decrease), and 5-HT content (5–27% decrease) in colitis mice.

Conclusion: The findings demonstrate that the anti-inflammatory effect of Myrobalan powder on TNBS - induced colitis may be mediated via reducing EC cell hyperplasia and 5-HT content. The important role of Myrobalan powder in regulating colonic EC cell number and 5-HT content may provide an alternative therapy for colonic inflammation.

Keywords: Colonic inflammation, enterochromaffin cell, serotonin, ulcerative colitis

References:

[1]. Bardazzi F, Odorici G, Virdi A, Antonucci VA, Tengattini V, Patrizi A, et al. Autoantibodies in psoriatic patients treated with anti-TNF-a therapy. J Dtsch Dermatol Ges 2014;12:401-6.

[2]. Bischoff SC, Mailer R, Pabst O, Weier G, Sedlik W, Li Z, et al. Role of serotonin in intestinal inflammation: Knockout of serotonin reuptake transporter exacerbates 2,4,6-trinitrobenzene sulfonic acid colitis in mice. Am J PhysiolGastrointest Liver Physiol 2009; 296:G685-95.

[3]. Costedio MM, Coates MD, Danielson AB, Buttolph TR 3rd, Blaszyk HJ, Mawe GM, et al. Serotonin signaling in diverticular disease. J GastrointestSurg 2008; 12: 1439-45.

[4]. Danese S. New therapies for inflammatory bowel disease: From the bench to the bedside. Gut 2012; 61:918-32.

[5]. Ghia JE, Li N, Wang H, Collins M, Deng Y, El-Sharkawy RT, et al. Serotonin has a key role in pathogenesis of experimental colitis. Gastroenterology 2009; 137:1649-60.

[6]. Haub S, Ritze Y, Bergheim I, Pabst O, Gershon MD, Bischoff SC. Enhancement of intestinal inflammation in mice lacking interleukin 10 by deletion of the serotonin reuptake transporter. NeurogastroenterolMotil 2010;22:826-34.

[7]. Levin AD, van den Brink GR. Selective inhibition of mucosal serotonin as treatment for IBD? Gut 2014; 63:866-7.

[8]. Margolis KG, Pothoulakis C. Serotonin has a critical role in the pathogenesis of experimental colitis. Gastroenterology 2009; 137:1562-6.

[9]. Margolis KG, Stevanovic K, Li Z, Yang QM, Oravecz T, Zambrowicz B, et al. Pharmacological reduction of mucosal but not neuronal serotonin opposes inflammation in mouse intestine. Gut 2014; 63:928-37.

[10]. Morris GP, Beck PL, Herridge MS, Depew WT, Szewczuk MR, Wallace JL. Hapten-induced model of chronic inflammation and ulceration in the rat colon. Gastroenterology 1989; 96: 795-803.

[11]. Margolis KG, Stevanovic K, Li Z, Yang QM, Oravecz T, Zambrowicz B, et al. Pharmacological reduction of mucosal but not neuronal serotonin opposes inflammation in mouse intestine. Gut 2014;63:928-37.

[12]. Spiller R. Serotonin and GI clinical disorders. Neuropharmacology 2008; 55:1072-80.

[13]. Xu XR, Liu CQ, Feng BS, Liu ZJ. Dysregulation of mucosal immune response in pathogenesis of inflammatory bowel disease. World J Gastroenterol 2014; 20: 3255-64.

[14]. Zhang YZ, Li YY. Inflammatory bowel disease: Pathogenesis. World J Gastroenterol 2014; 20: 91-9.

[15]. Zheng X, Kang A, Dai C, Liang Y, Xie T, Xie L, et al. Quantitative analysis of neurochemical panel in rat brain and plasma by liquid chromatography-tandem mass spectrometry. Anal Chem 2012;84: 10044-51.