Abstract

BackgroundCrohn’s disease (CD) is a chronic relapsing form of inflammatory bowel disease, seriously threatening human beings health. However, the pathogenesis of CD is still unclear and there is no specific effective drug for treatment of CD. Resina Donis (RD) obtained from Dracaena cochinchinensis (Lour.) S. C. Chen (Liliaceae), has been used for the treatment of CD clinically. Loureirin B (LB) is one of the most important chemical compositions and physiologically active ingredients of resina draconis. It has the molecular structure propan-1-one, 1-(4-hydroxyphenyl)-3-(2,4,6-trimethoxyphenyl)-1-(4-hydroxyphenyl)-3-(2,4,6-trimethoxyphenyl) propan-1-one. The aim of this study was to investigate the effect of LB on CD and explore the underlying mechanisms.Methods and resultsIn this study, the result demonstrated that LB prolonged the survival time of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced rats and alleviated colonic damage in a dose dependent manner. Besides, LB remarkably ameliorated TNBS-induced inflammatory response via regulation of cytokines in the colonic tissues. Moreover, LB could reverse the established fibrosis and impede the accumulation infiltration, and improve the apoptosis induced by TNBS in a dose dependent manner. Further, LB dramatically suppressed TNBS-induced the activation of IL-6/STAT3/NF-κB signaling pathway.ConclusionsThese findings suggested that LB could be beneficial regarding ameliorating TNBS-induced CD, which may represent a novel approach to treat CD and provide an alternative choice for disorders associated with CD.

Highlights

  • Crohn’s disease (CD) is a chronic relapsing form of inflammatory bowel disease, seriously threatening human beings health

  • These findings suggested that Loureirin B (LB) could be beneficial regarding ameliorating trinitrobenzene sulfonic acid (TNBS)-induced CD, which may represent a novel approach to treat CD and provide an alternative choice for disorders associated with CD

  • Interaction between antigen presenting cells in intestinal mucosal immune system and local bacterial flora leads to the uncontrolled activation of mucosal ­CD4+ T cells, and sustained release of inflammatory factors such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-12, IL-23, IL-27 and IL-17, which are important factors resulting in intestinal injury in CD patients [10, 11]

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Summary

Introduction

Crohn’s disease (CD) is a chronic relapsing form of inflammatory bowel disease, seriously threatening human beings health. In the pathological state of CD, ­CD4+ T cells exhibit apoptosis resistance, and the accumulation of C­ D4+ T cells in inflammatory sites mainly depends on anti-apoptotic IL-6 transmembrane signaling pathway [12]. T cell apoptosis resistance and aggregation eventually lead to a vicious cycle of chronic inflammation, which can be effectively blocked by anti-IL-6 receptor antibody, indicating that IL-6/STAT3 signaling pathway plays a central role in apoptosis resistance in the pathological state of CD [15]. Recent studies have found that IL-6 signaling pathway plays an important role in the occurrence and differentiation of Th17, suggesting that IL-6/STAT3 trans-membrane signaling pathway is essential for T cells apoptosis resistance and type Th17 immune reaction [16, 17]. In inflammatory cells, the inappropriate activation of nuclear factor-кB (NF-кB) is the key transcription factor that regulates the expression of the inflammatory mediators, which is related to the occurrence and development of CD inflammation [18]

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