Abstract
ABSTRACTThe primary aim of this study was to determine whether the oral administration of AD-lico™, a functional extract from Glycyrrhiza inflata in combination with 5-aminosalicylic acid (5-ASA) could ameliorate the inflammatory symptoms in dextran sulfate sodium (DSS)-induced colitis in rodents. This DSS rodent model is used to study drug candidates for colitis, as part of the spectrum of diseases falling under the inflammatory bowel disease (IBD) category. Here, with oral AD-lico™ administration, there was a substantial disruption of the colonic architectural changes due to DSS and a significant reduction in colonic myeloperoxidase (MPO) activity, a marker of colitis. In the same samples, there were also reduced levels of colonic and serum IL-6 in the oral AD-lico™ treated rats. This study also addressed the possible mechanisms for AD-lico™ mediated changes on colonic inflammation markers. These included the observations that AD-lico™ dampened the IL-6 proinflammatory-signaling pathway in THP-1 human monocytic cells and reduced the TNFα-mediated upregulation of surface adhesion molecule ICAM-1 in human umbilical vein endothelial cells (HUVECs). Finally, it was shown that AD-lico™ could be combined with 5-ASA in reducing the inflammatory markers for colorectal sites affected by colitis, a first study of its kind for a combination therapy.
Highlights
As part of the treatment strategy for patients with inflammatory bowel disease (IBD), inhibitors of tumor necrosis factor alpha (TNFα) have been shown to be effective in reducing their symptoms associated with IBD
The conditions falling under the designation of inflammatory bowel disease (IBD) include ulcerative colitis (UC) and Crohn’s disease (CD)
On whether Glycyrrhiza extracts or its constituents could regulate intestinal inflammation and to explore the potential benefits of AD-licoTM derived from Glycyrrhiza extracts in UC therapy, we examined its effects on dextran sulfate sodium (DSS)-induced colitis in a rat model and in combination with 5-aminosalicylic acid (5-ASA)
Summary
As part of the treatment strategy for patients with inflammatory bowel disease (IBD), inhibitors of tumor necrosis factor alpha (TNFα) have been shown to be effective in reducing their symptoms associated with IBD. 30% of patients resistant to standard therapy are refractory to TNFα blocking agents. Of those that do respond, an excess of 50% stop responding after one year on those targeted agents (Ghosh and Panaccione 2010). The conditions falling under the designation of inflammatory bowel disease (IBD) include ulcerative colitis (UC) and Crohn’s disease (CD). These are chronic conditions that are remitting and relapsing (Strober et al 2002). The inflammatory mediators in UC include produced reactive oxygen species (ROS) such as nitric oxide (NO) (Kolios et al 2004; Araki et al 2006), prostaglandins (PG) (Singer et al 1998; Bonner 2002) and cytokines such as interleukin (IL)-6, tumor necrosis (TNF)-α and interferon (IFN)-γ (Atreya and Neurath 2005; Rojas-Cartagena et al 2005; Ito et al 2006)
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