Increasing endogenous 2‐arachidonoylglycerol levels counteracts colitis and related systemic inflammation
@article{Alhouayek2011IncreasingE2, title={Increasing endogenous 2‐arachidonoylglycerol levels counteracts colitis and related systemic inflammation}, author={Mireille Alhouayek and Didier M. Lambert and Nathalie M. Delzenne and Patrice D Cani and Giulio G. Muccioli}, journal={The FASEB Journal}, year={2011}, volume={25}, pages={2711 - 2721} }
Inflammatory bowel diseases (IBDs) are chronic inflammatory conditions for which new therapeutic approaches are needed. Genetic and pharmacological data point to a protective role of CB1 and CB2 cannabinoid receptor activation in IBD experimental models. Therefore, increasing the endogenous levels of 2‐arachidonoylglycerol, the main full agonist of these receptors, should have beneficial effects on colitis. 2‐Arachidonoylglycerol levels were raised in the trinitrobenzene sulfonic acid (TNBS…
177 Citations
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- BiologyFASEB journal : official publication of the Federation of American Societies for Experimental Biology
- 2018
PGD2‐G could be one of the products from the COX‐2/prostaglandin D synthase axis to exert beneficial effects in colitis, and is shown to be an agonist of the PGD2 receptor 1 (DP1) and that some of the effects of PGD 2‐G were blocked by antagonism of peroxisome proliferator‐activated receptor γ and DP1.
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- BiologyProceedings of the National Academy of Sciences
- 2013
In macrophages, the newly characterized enzyme α/β-hydrolase domain 6 (ABHD6) controls 2-arachidonoylglycerol (2-AG) levels and thus its pharmacological effects, and this points to ABHD6 as an interesting therapeutic target that should be relevant in treating inflammation-related conditions, and proposes PGD2-G as a bioactive lipid with potential anti-inflammatory properties in vivo.
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Elevation of arachidonoylethanolamide levels by activation of the endocannabinoid system protects against colitis and ameliorates remote organ lesions in mice.
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Modulation of the ECS was efficient in ameliorating colitis and increasing the survival rate of the mice, and reducing remote organ changes induced by colitis, suggesting that modulation ofThe ECS is a potential therapeutic approach for IBDs and the associated remote organ lesions.
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