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Research ArticleCELLULAR AND MOLECULAR

Inhibition of Rat C6 Glioma Cell Proliferation by Endogenous and Synthetic Cannabinoids. Relative Involvement of Cannabinoid and Vanilloid Receptors

Stig O. P. Jacobsson, Thomas Wallin and Christopher J. Fowler
Journal of Pharmacology and Experimental Therapeutics December 2001, 299 (3) 951-959;
Stig O. P. Jacobsson
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Thomas Wallin
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Christopher J. Fowler
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Abstract

The effects of the endocannabinoids anandamide (AEA) and 2-arachidonoylglycerol (2-AG) upon rat C6 glioma cell proliferation were examined and compared with a series of synthetic cannabinoids and related compounds. Cells were treated with the compounds each day and cell proliferation was monitored for up to 5 days of exposure. AEA time- and concentration-dependently inhibited C6 cell proliferation. After 4 days of treatment, AEA and 2-AG inhibited C6 cell proliferation with similar potencies (IC50 values of 1.6 and 1.8 μM, respectively), whereas palmitoylethanolamide showed no significant antiproliferative effects at concentrations up to 10 μM. The antiproliferative effects of both AEA and 2-AG were blocked completely by a combination of antagonists at cannabinoid receptors (SR141716A and SR144528 or AM251 and AM630) and vanilloid receptors (capsazepine) as well as by α-tocopherol (0.1 and 10 μM), and reduced by calpeptin (10 μM) and fumonisin B1 (10 μM), but not byl-cycloserine (1 and 100 μM). CP 55,940, JW015, olvanil, and arachidonoyl-serotonin were all found to affect C6 glioma cell proliferation (IC50 values of 5.6, 3.2, 5.5, and 1.6 μM, respectively), but the inhibition could not be blocked by cannabinoid + vanilloid receptor antagonists. It is concluded that the antiproliferative effects of the endocannabinoids upon C6 cells are brought about by a mechanism involving combined activation of both vanilloid receptors and to a lesser extent cannabinoid receptors, and leading to oxidative stress and calpain activation. However, there is at present no obvious universal mechanism whereby plant-derived, synthetic, and endogenous cannabinoids affect cell viability and proliferation.

Footnotes

  • This work was supported by MFR Grant 12158 from the Swedish Research Council and research funds of the Medical Odontological Faculty, Umeå University, Umeå, Sweden.

  • Abbreviations:
    Δ9-THC
    Δ9-tetrahydrocannabinol
    CB
    cannabinoid
    AEA
    N-arachidonoylethanolamide (anandamide)
    2-AG
    2-arachidonoylglycerol
    PEA
    palmitoylethanolamide
    AA-5-HT
    arachidonoyl-serotonin
    ACEA
    arachidonyl-2′-chloroethylamide/(all Z)-N-(2-cycloethyl)-5,8,11,14-eicosatetraenamide
    ANOVA
    analysis of variance
    meAEA
    R-(+)-methanandamide
    VR
    vanilloid receptor
    FAAH
    fatty acid amidohydrolase
    • Received May 30, 2001.
    • Accepted August 28, 2001.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 299 (3)
Journal of Pharmacology and Experimental Therapeutics
Vol. 299, Issue 3
1 Dec 2001
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Research ArticleCELLULAR AND MOLECULAR

Inhibition of Rat C6 Glioma Cell Proliferation by Endogenous and Synthetic Cannabinoids. Relative Involvement of Cannabinoid and Vanilloid Receptors

Stig O. P. Jacobsson, Thomas Wallin and Christopher J. Fowler
Journal of Pharmacology and Experimental Therapeutics December 1, 2001, 299 (3) 951-959;

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Research ArticleCELLULAR AND MOLECULAR

Inhibition of Rat C6 Glioma Cell Proliferation by Endogenous and Synthetic Cannabinoids. Relative Involvement of Cannabinoid and Vanilloid Receptors

Stig O. P. Jacobsson, Thomas Wallin and Christopher J. Fowler
Journal of Pharmacology and Experimental Therapeutics December 1, 2001, 299 (3) 951-959;
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