AI Article Synopsis

  • The study investigated whether AD-lico™, a functional extract, combined with 5-aminosalicylic acid (5-ASA) could reduce inflammation in a rodent model of colitis induced by dextran sulfate sodium (DSS).
  • Results showed that oral administration of AD-lico™ led to significant improvements, including reduced colonic architectural damage, lower colonic myeloperoxidase activity, and decreased levels of IL-6 in treated rats.
  • Additionally, the research explored the mechanisms behind these effects, revealing that AD-lico™ inhibited pro-inflammatory pathways in human cells and demonstrated efficacy when used alongside 5-ASA for targeting inflammatory markers in colitis.

Article Abstract

The primary aim of this study was to determine whether the oral administration of AD-lico™, a functional extract from 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6138317PMC
http://dx.doi.org/10.1080/19768354.2018.1476409DOI Listing

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