in vivo Posted March 3, 2014 Report Share Posted March 3, 2014 (edited) Abstract Activation of cannabinoid receptors (CBs) by endocannabinoids impacts on a number of gastrointestinal functions. Recent data indicate that CB1 agonists improve 2,4-dinitrobenzene sulfonic acid-induced colitis in mice, thus suggesting a role for the endocannabinoid agonist anandamide (AEA) in protecting the gut against inflammation. We here examined the gut endocannabinoid system in inflammatory bowel disease (IBD) patients, and investigated the ex vivo and in vitro effects of the non-hydrolysable AEA analog methanandamide (MAEA) on the mucosal proinflammatory response. The content of AEA, but not of 2-arachidonoyl-glycerol and N-palmitoylethanolamine, was significantly lower in inflamed than uninflamed IBD mucosa, and this was paralleled by lower activity of the AEA-synthesizing enzyme N-acyl-phosphatidylethanolamine-specific phospholipase D and higher activity of the AEA-degrading enzyme fatty acid amide hydrolase. MAEA significantly downregulated interferon-γ and tumor necrosis factor-α secretion by both organ culture biopsies and lamina propria mononuclear cells. Although these results are promising, further studies are needed to determine the role of cannabinoid pathways in gut inflammation. http://www.nature.com/mi/journal/v4/n5/full/mi201118a.html This indicates a possible correlation between low anandamide levels in inflamed IBD mucosa. Since THC has some similar characteristics to anandamide, its already known effectiveness might be in association with hitting the CB1 receptors that line the gut in place of anandamide, similar to what was mentioned the other day. CBD also raises anandamide levels. So does dietary linoleic acid. There are many ways to modulate endogenous cannabinoids levels, and there is much therapeutic benefit to be gained by doing so, in some cases. Edited March 3, 2014 by in vivo Quote Link to comment Share on other sites More sharing options...
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