CNR1 and colitis: Most probably, these effects would be related to cannabinoid receptors type 1 (CB1) activation that mediates essential protective signals and counteracts proinflammatory pathways, since it has been reported that the severity of two different experimental models of colitis, induced by the intrarectal infusion of 2,4-dinitrobenzene sulfonic acid (DNBS) or by oral administration of DSS, are higher in CB1-deficient mice (CB1(−/−)) than in wild-type [90].