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Review
. 2009 Mar;11(1):109-19.
doi: 10.1208/s12248-009-9084-5. Epub 2009 Feb 6.

Cannabinoids, Endocannabinoids, and Related Analogs in Inflammation

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Free PMC article
Review

Cannabinoids, Endocannabinoids, and Related Analogs in Inflammation

Sumner H Burstein et al. AAPS J. .
Free PMC article

Abstract

This review covers reports published in the last 5 years on the anti-inflammatory activities of all classes of cannabinoids, including phytocannabinoids such as tetrahydrocannabinol and cannabidiol, synthetic analogs such as ajulemic acid and nabilone, the endogenous cannabinoids anandamide and related compounds, namely, the elmiric acids, and finally, noncannabinoid components of Cannabis that show anti-inflammatory action. It is intended to be an update on the topic of the involvement of cannabinoids in the process of inflammation. A possible mechanism for these actions is suggested involving increased production of eicosanoids that promote the resolution of inflammation. This differentiates these cannabinoids from cyclooxygenase-2 inhibitors that suppress the synthesis of eicosanoids that promote the induction of the inflammatory process.

Figures

Fig. 1
Fig. 1
Phytocannabinoids and analogs. THC and CBD are the principle examples of the 80 odd cannabinoids identified in Cannabis. Nabilone (Cesamet®) and ajulemic acid (AJA, CT-3, or IP-751) are synthetic analogs of THC that have shown therapeutic effects in humans
Fig. 2
Fig. 2
Chemical structures of endogenous compounds. Anandamide and 2-AG are the two most studied endocannabinoids and each binds to and activates the cannabinoid receptors. N-Arachidonyl glycine is the best-studied member of the elmiric acid family of lipoamino acids and does not bind to CB1. Using a proposed nomenclature system (vide infra), it would be called EMA-1 (20:4)
Fig. 3
Fig. 3
The in vivo effect of EMA-1(20:4) on cell migration (a) vs. 15d-PGJ2 production by mouse peritoneal macrophages (b). CD-1 male mice 18–20 g body weight were administered the above indicated treatments p.o. and after 30 min, injected i.p. with 1 ml 8% BBL Fluid Thioglycollate Medium. a Cells were harvested by peritoneal lavage after 3 h, exposed to lysing buffer for 2 min to remove erythrocytes, resuspended in phosphate buffered saline/bovine serum albumin and an aliquot subjected to the cell TiterGlo assay with four replicates for each sample. b The remaining cells were suspended in 1 ml minimum essential medium and plated onto 32 wells of a 48-well dish (eight wells/group). The plates were incubated for 18 h, the media harvested, centrifuged, and assayed for 15d-PGJ2 by enzyme-linked immunosorbent assay (Assay Designs). Numbers of adherent cells were obtained using the TiterGlo assay that measures ATP levels. The values shown are the prostaglandin concentrations (pg/ml) divided by number of adherent cells
Fig. 4
Fig. 4
Inhibition of proliferation of human breast cancer cells (HTB-126) vs. normal (HTB-125) cells. HTB-126™ (Hs 578T) cell strain was derived from a carcinoma of the breast. It was originated by Vuong et al. (112) along with the Hs 578Bst (HTB-125™), which is a normal fibroblast-like line from the same patient. The donor was a 74-year-old female Caucasian. Hs 578Bst was derived from normal breast tissue peripheral to an infiltrating ductal carcinoma that was the source for HTB-126. The cell proliferation assay, which measures ATP levels, was performed at 48 h following drug treatment and the values are expressed as a percentage of the vehicle-treated wells
Fig. 5
Fig. 5
Structures of noncannabinoid plant constituents

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