PALMITOYLETHANOLAMIDE AND MINOCYCLINE SUPRESS NITRIC OXIDE-INDUCED PROSTAGLANDIN E2 RELEASE FROM TRIGEMINAL SATELLITE GLIAL CELLS IN VITRO

At Florence, Italy the EFIC Congress 2013 “Pain in Europe VIII”, takes place in October 9-12. The Congress will bring together over 4,000 pain specialists for a multidisciplinary forum that will focus on the latest developments in the study and treatment of acute or chronic and recurrent pain. At this congress palmitoylethaolamide also played a role and an interesting topic was presented:

PALMITOYLETHANOLAMIDE AND MINOCYCLINE SUPRESS NITRIC OXIDE-INDUCED PROSTAGLANDIN E2 RELEASE FROM TRIGEMINAL SATELLITE GLIAL CELLS IN VITRO

presented by Drs Parisa P. Gazerani, J.C. Laursen and B.E. Cairns of the Department of Health Science and Technology, Aalborg University, Aalborg, Denmark, and the Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, BC, Canada

We quote from the presentation:

Background and aims: Activated trigeminal satellite glial cells (SGCs) are capable of releasing substances that may contribute to craniofacial nociceptive transmission. Therefore, modulation of SGC activation and substance release may offer a novel strategy for management of such pain conditions. The present study aimed at testing whether palmitoylethanolamide (PEA) and minocycline, which both have glial modulatory properties, could interfere with prostaglandin E2 (PGE2) release from activated trigeminal SGCs.

Methods: Trigeminal SGCs were isolated from adult male Sprague-Daley rats (n=15). Initially, the time- and concentration-dependent effect of the nitric oxide donator Diethylenetriamine/nitric oxide (DETA/NO) on PGE2 release was investigated by applying 0, 10, 100, and 1000 µM DETA/NO for 4, 8, and 24h. Subsequently, SGCs were pretreated for 24h with 0.1, 1, or 10 µM PEA or minocycline and then stimulated with 1000 µM DETA/NO for 8h.

Results: There was a time- and concentration-dependent effect of DETA/NO on PGE2 release, which was most pronounced after 8h of treatment with 1000 µM. PEA significantly (p< 0.05) reduced this DETA/NO-evoked PGE2 release from 95.3±13.5 pg/ml to 78.7±8.0, 73.0±5.7, and 70.8±5.4 pg/ml for 0.1, 1, and 10 µM, respectively. Similarly, 10 µM Minocycline reduced PGE2 release from 78.7±11.6 pg/ml to 50.0±8.0 pg/ml (p< 0.05).

Conclusions: The results indicate that PEA and minocycline suppress PGE2 release from trigeminal SGCs with comparable efficacy. Since PGE2 can alter neuronal excitability within the trigeminal ganglion to facilitate nociception, suppression of PGE2 release from trigeminal SGCs by PEA and minocycline could offer additional strategies to treat craniofacial pain.

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