290 , H2528H2534 (2006)

If the receptor is activated, the cell releases fewer pro-inflammatory signal substances, or cytokines. In a related study undertaken at the University of Milan, Italy, Oral anti-inflammatory activity of cannabidiol, a non-psychoactive constituent of cannabis, in acute carrageenan-induced inflammation in the rat paw (Naunyn-Schmiedebergs Archives of Pharmacology, March 2004), scientists found that CBD reduced induced inflammation in rat paws: There were decreases in PGE2 (prostaglandin E2) plasma levels, tissue COX (cyclooxygenase) activity, production of oxygen-derived free radicals , and NO (nitric oxide) after three doses of cannabidiolIn conclusion, oral cannabidiol has a beneficial action on two symptoms of established inflammation: edema (fluid retention) and hyperalgesia (increased sensitivity to pain). Another study found the effectiveness of yet another lesser known cannabinoid, CBC or cannabichromene, on fighting inflammation: Inhibitory effect of cannabichromene, a major non-psychotropic cannabinoid extracted from Cannabis sativa, on inflammation-induced hypermotility in mice (British Journal of Pharmacology, June 2012) CBC selectively reduces inflammation-induced hypermotility in vivo in a manner that is not dependent on cannabinoid receptors or TRPA1. And finally, a study undertaken in 2004 by the Japanese Pharmacological Society, New Perspectives in the Studies on Endocannabinoid and Cannabis: 2-Arachidonoylglycerol as a Possible Novel Mediator of Inflammation (Journal of Pharmacological Sciences, Oct 2004) points to yet another of the lesser known cannabinoids, 2-AG, as a possible anti-inflammatory: It is apparent that 2-AG plays an important part during the course of a variety of inflammatory reactions, such as acute inflammation and allergic inflammation in vivo, yet the details of the mechanism as well as the mode of action of 2-AG remain to be clarified

The authors declare no other conflicts of interest
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