Abstract
Anandamide (AEA) exhibits anti-inflammatory effects. However, its role in the periodontal field remains unknown. Here, we found that gingival crevicular fluid contained a detectable level of AEA. The cannabinoid receptors CB1 and CB2 were expressed by human gingival fibroblasts (HGFs), and markedly upregulated under pathological conditions. AEA significantly reduced the production of pro-inflammatory mediators (IL-6, IL-8 and MCP-1) induced by Porphyromonas gingivalis LPS in HGFs, and this effect was attenuated by AM251 and SR144528, selective antagonists of CB1 and CB2, respectively. Moreover, AEA completely blocked LPS-triggered NF-kappaB activation, implying that AEA may regulate hyperinflammatory reactions in periodontitis.
MeSH terms
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Arachidonic Acids / metabolism*
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Cannabinoid Receptor Modulators / metabolism*
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Cells, Cultured
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Endocannabinoids*
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Fibroblasts / cytology
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Fibroblasts / drug effects
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Fibroblasts / metabolism
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Gingiva / chemistry
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Gingiva / cytology
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Gingiva / metabolism*
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Gingiva / pathology
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Gingival Crevicular Fluid / chemistry
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Gingivitis / immunology
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Gingivitis / pathology
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Humans
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Lipopolysaccharides / pharmacology
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NF-kappa B / antagonists & inhibitors
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NF-kappa B / metabolism*
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Periodontitis* / immunology
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Periodontitis* / pathology
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Polyunsaturated Alkamides
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Receptor, Cannabinoid, CB1 / genetics
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Receptor, Cannabinoid, CB1 / metabolism
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Receptor, Cannabinoid, CB2 / genetics
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Receptor, Cannabinoid, CB2 / metabolism
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Signal Transduction / physiology*
Substances
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Arachidonic Acids
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Cannabinoid Receptor Modulators
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Endocannabinoids
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Lipopolysaccharides
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NF-kappa B
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Polyunsaturated Alkamides
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Receptor, Cannabinoid, CB1
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Receptor, Cannabinoid, CB2
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anandamide