Abnormal cannabidiol attenuates experimental colitis in mice,promotes wound healing and inhibits neutrophil recruitment

Background: non-psychotropic atypical cannabinoids have therapeutic potential in a variety of inflammatory conditions including those of the gastrointestinal tract. here we examined the effects of the atypical cannabinoid abnormal cannabidiol (abn-cbd) on wound healing,inflammatory cell recruitment and colitis in mice. methods: colitis was induced in cd1 mice by a single intrarectal administration of trinitrobenzene sulfonic acid (tnbs,4 mg/100 μl in 30 % ethanol) and abn-cbd and/or the antagonists o-1918 (abd-cbd),am251 (cb1 receptor) and am630 (cb2 receptor),were administered intraperitoneally (all 5 mg/kg,twice daily for 3 days). the degree of colitis was assessed macro- and microscopically and tissue myeloperoxidase activity was determined. the effects of abn-cbd on wound healing of endothelial and epithelial cells (lovo) were assessed in a scratch injury assay. human neutrophils were employed in transwell assays or perfused over human umbilical vein endothelial cells (huvec) to study the effect of abn-cbd on neutrophil accumulation and transmigration. results: tnbs-induced colitis was attenuated by treatment with abn-cbd. histological,macroscopic colitis scores and tissue myeloperoxidase activity were significantly reduced. these effects were inhibited by o-1918,but not by am630,and only in part by am251. wound healing of both huvec and lovo cells was enhanced by abn-cbd. abn-cbd inhibited neutrophil migration towards il-8,and dose-dependently inhibited accumulation of neutrophils on huvec. conclusions: abn-cbd is protective against tnbs-induced colitis,promotes wound healing of endothelial and epithelial cells and inhibits neutrophil accumulation on huvec monolayers. thus,the atypical cannabinoid abn-cbd represents a novel potential therapeutic in the treatment of intestinal inflammatory diseases. © 2016 the author(s).