Adelmidrol exerts important anti-inflammatory effects that are partly dependent on PPARγ. Adelmidrol reduces NF-κB translocation, and COX-2 expression.
Adelmidrol is a palmitoylethanolamide analogue. Adelmidrol reduces NF-κB translocation, COX-2, and p-ERK expression; proinflammatory cytokine release; and the incidence of nitrotyrosine and poly(ADP)ribose in the colon[1].
Adelmidrol (10 mg/kg, o.s.) reduces significantly the degree and severity of the macroscopic and histologic signs of colon injury. Moreover, 4 days after colitis induced by dinitrobenzene sulfonic acid (DNBS) treatment, all mice have diarrhea and a reduction in body weight (compared with the sham groups). Adelmidrol (10 mg/kg, o.s.) treatment significantly reduces the loss of body weight. The inflammatory bowel disease (IBD) induced by DNBS intrarectally administered is also characterized by an augmentation in myeloperoxidase (MPO) activity, an indicator of neutrophil accumulating in the colon. This is consistent with light microscopic observations showing the colon of vehicle-treated DNBS mice to contain a large number of neutrophils. In contrast, Adelmidrol (10 mg/kg, o.s.) significantly reduces the degree of polymorphonuclear cell infiltration (determined as reduction in MPO activity) in inflamed colon[1].
[1]. Cordaro M, et al. Adelmidrol, a Palmitoylethanolamide Analogue, as a New Pharmacological Treatment for the Management of Inflammatory Bowel Disease. Mol Pharmacol. 2016 Nov;90(5):549-561.