Therapeutic efficacy and mechanism of water-soluble extracts of Banxiaxiexin decoction on BALB/c mice with oxazolone-induced colitis

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Abstract

The aim of the present study was to investigate the therapeutic effects of water-soluble extracts of Banxiaxiexin decoction, a classical traditional Chinese medicine formulation, on BALB/c mice with experimentally induced ulcerative colitis (UC). Water-soluble extracts of Banxiaxiexin decoction were intragastrically administered to BALB/c mice with oxazolone (OXA)-induced colitis. Sulfasalazine (SASP) was administered intragastrically to OXA-treated mice to establish the SASP group (positive control). Following drug administration, the disease activity index (DAI) and the histopathological inflammation score were recorded. In addition, the expression levels of interleukin (IL)-5 and IL-13 mRNA in the colonic tissue were determined by fluorescent quantitative polymerase chain reaction. The DAI and histopathological inflammation score of the model group were significantly greater compared with those of the control group, and the mRNA expression levels of IL-5 and IL-13 in the colonic tissue were also significantly higher in the model group compared with those in the control group. The intragastric administration of water-soluble extracts of Banxiaxiexin decoction significantly lowered the DAI and histopathological inflammation score. The mRNA expression levels of IL-5 and IL-13 in the colonic tissue were also significantly lowered. The therapeutic effect of Banxiaxiexin decoction was found to be comparable to that of SASP. In conclusion, the results from the present study demonstrate that water-soluble extracts of the traditional Chinese medicine formulation Banxiaxiexin decoction have a therapeutic effect on BALB/c mice with OXA-induced colitis.

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Chemically induced mouse models of intestinal inflammation.

Stefan Wirtz, Clemens F. Neufert, Benno Weigmann … (2007)

Animal models of intestinal inflammation are indispensable for our understanding of the pathogenesis of Crohn disease and ulcerative colitis, the two major forms of inflammatory bowel disease in humans. Here, we provide protocols for establishing murine 2,4,6-trinitro benzene sulfonic acid (TNBS)-, oxazolone- and both acute and chronic dextran sodium sulfate (DSS) colitis, the most widely used chemically induced models of intestinal inflammation. In the former two models, colitis is induced by intrarectal administration of the covalently reactive reagents TNBS/oxazolone, which are believed to induce a T-cell-mediated response against hapten-modified autologous proteins/luminal antigens. In the DSS model, mice are subjected several days to drinking water supplemented with DSS, which seems to be directly toxic to colonic epithelial cells of the basal crypts. The procedures for the hapten models of colitis and acute DSS colitis can be accomplished in about 2 weeks but the protocol for chronic DSS colitis takes about 2 months.

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Disparate CD4+ lamina propria (LP) lymphokine secretion profiles in inflammatory bowel disease. Crohn's disease LP cells manifest increased secretion of IFN-gamma, whereas ulcerative colitis LP cells manifest increased secretion of IL-5.

I. Fuss, M Neurath, M Boirivant … (1996)

In this study, we investigate whether human inflammatory bowel disease (IBD) (ulcerative colitis and Crohn's disease) is associated with altered lymphokine secretion profiles, as recently found in various animal models of chronic intestinal inflammation. In initial studies, we determined the proliferative responses of purified lamina propria (LP) CD4+ T cells from patients with IBD under defined conditions of T cell stimulation. We found that IBD LP CD4+ T cells in comparison with control LP CD4+ T cells have diminished TCR/CD3 pathway proliferative responses, whereas CD2/CD28 accessory pathway proliferative responses are relatively preserved. In further studies centering on lymphokine production, we showed that LP T cells from inflamed Crohn's disease mucosa manifest increased IFN-gamma secretion compared with control LP T cells, particularly when stimulated via the CD2/CD28 pathway. Subsequent ELISPOT analysis indicated that this was due to an increased number of IFN-gamma-secreting CD4+ T cells. In contrast, IL-4 and IL-5 production by Crohn's disease LP T cells was decreased compared with that of control LP T cells. Of interest, IL-2 production by Crohn's disease LP T cells was also reduced, as was IL-2 production by peripheral blood T cells. In parallel studies, LP T cells from inflamed ulcerative colitis mucosa stimulated via either the TCR/CD3/CD28 or CD2/CD28 produced increased amounts of IL-5, again when measured either as secreted IL-5 or by ELISPOT analysis. Such increased IL-5 production was not associated with increased IL-4 secretion and, in contrast to Crohn's disease, ulcerative colitis LP T cell production of IL-2 and IFN-gamma was normal. Taken together, these studies provide strong evidence that the immunopathologic process characteristic of the two major forms of IBD is associated with very different cytokine secretion patterns. These different patterns may determine the type of inflammatory process present.

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Oxazolone colitis, a Th2 colitis model resembling ulcerative colitis, is mediated by IL-13-producing NK-T cells.

Frank Heller, Ivan Fuss, Edward Nieuwenhuis … (2002)

Oxazolone colitis (OC) is an experimental colitis that has a histologic resemblance to human ulcerative colitis. Here we show that IL-13 production is a significant pathologic factor in OC since its neutralization by IL-13Ralpha2-Fc administration prevents colitis. We further show that OC is mediated by NK-T cells since it can be induced neither in mice depleted of NK-T cells nor in mice that cannot present antigen to NK-T cells and mice lacking an NK-T cell-associated TCR. Finally, we show that NK-T cells are the source of the IL-13, since they produce IL-13 upon stimulation by alpha-galactosylceramide, an NK-T cell-specific antigen. These data thus describe a cellular mechanism underlying an experimental colitis that may explain the pathogenesis of ulcerative colitis.

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Author and article information

Journal

Journal ID (nlm-ta): Exp Ther Med

Journal ID (iso-abbrev): Exp Ther Med

Journal ID (publisher-id): ETM

Title: Experimental and Therapeutic Medicine

Publisher: D.A. Spandidos

ISSN (Print): 1792-0981

ISSN (Electronic): 1792-1015

Publication date (Print): October 2014

Publication date (Electronic): 08 August 2014

Publication date PMC-release: 08 August 2014

Volume: 8

Issue: 4

Pages: 1201-1204

Affiliations

[1 ]Department of Gastroenterology, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, P.R. China

[2 ]Department of Pathology, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, P.R. China

Author notes

Correspondence to: Dr Xuewei Wang, Department of Gastroenterology, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, 164 Lanxi Road, Shanghai 200062, P.R. China, wangxw1976@ 123456hotmail.com

Article

Publisher ID: etm-08-04-1201

DOI: 10.3892/etm.2014.1890

PMC ID: 4151664

PubMed ID: 25187824

SO-VID: 59496824-6286-49c8-9787-b2b3c1a39383

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This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.

Therapeutic efficacy and mechanism of water-soluble extracts of Banxiaxiexin decoction on BALB/c mice with oxazolone-induced colitis

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Karger: Gastroenterology

Most cited references 16

Chemically induced mouse models of intestinal inflammation.

Disparate CD4+ lamina propria (LP) lymphokine secretion profiles in inflammatory bowel disease. Crohn's disease LP cells manifest increased secretion of IFN-gamma, whereas ulcerative colitis LP cells manifest increased secretion of IL-5.

Oxazolone colitis, a Th2 colitis model resembling ulcerative colitis, is mediated by IL-13-producing NK-T cells.

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