Ajulemic acid, a nonpsychoactive cannabinoid acid, induces apoptosis in human T lymphocytes

Oral administration of ajulemic acid (AjA), a synthetic nonpsychoactive cannabinoid acid, prevents joint cartilage and bone damage in an experimental model of arthritis in rats. Joint tissue injury in patients with rheumatoid arthritis (RA) is due in part to activation of T lymphocytes in the synovi...

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Publié dans:Clinical immunology (Orlando, Fla.). - 1999. - 108(2003), 2 vom: 15. Aug., Seite 95-102
Auteur principal: Bidinger, Bonnie (Auteur)
Autres auteurs: Torres, Roxabella, Rossetti, Ronald G, Brown, Lisa, Beltre, Rosa, Burstein, Sumner, Lian, Jane B, Stein, Gary S, Zurier, Robert B
Format: Article
Langue:English
Publié: 2003
Accès à la collection:Clinical immunology (Orlando, Fla.)
Sujets:Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Annexin A5 Antirheumatic Agents Dronabinol 7J8897W37S CASP3 protein, human EC 3.4.22.- Caspase 3 plus... Caspases Fluorescein-5-isothiocyanate I223NX31W9 lenabasum OGN7X90BT8
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Résumé:Oral administration of ajulemic acid (AjA), a synthetic nonpsychoactive cannabinoid acid, prevents joint cartilage and bone damage in an experimental model of arthritis in rats. Joint tissue injury in patients with rheumatoid arthritis (RA) is due in part to activation of T lymphocytes in the synovium, and T lymphocytes in synovium of RA patients are resistant to apoptosis. Thus, a potential mechanism whereby AjA prevents joint tissue injury in the animal model might be enhanced apoptosis of T lymphocytes. Apoptosis of human T cells in vitro was assessed by Annexin V expression, caspase-3 activity, DNA fragmentation, and microscopy. AjA induced apoptosis of T cells in a dose- and time-dependent manner. Apoptosis preceded loss of cell viability by trypan blue dye exclusion, confirming that cell loss was due to programmed cell death rather than necrosis. A nontoxic compound such as AjA may be a useful therapeutic agent for patients with diseases such as RA which are characterized by T-cell-driven chronic inflammation and tissue injury
Description:Date Completed 01.10.2003
Date Revised 31.12.2020
published: Print
Citation Status MEDLINE
ISSN:1521-7035