Effect of Myrrh Oil on Il-1beta Stimulation of Nf-kappab Activation and Pge(2) Production in Human Gingival Fibroblasts and Epithelial Cells.
From: Dental Research Center and Department of Periodontology, College of Dentistry, University of Tennessee Health Science Center, Memphis, TN 38163, USA. dtipton@utmem.edu
Toxicology in vitro : an international journal published in association with BIBRA
- Publish Date: Mar 2006
- ISSN: 0887-2333
- Volume: 20
- Issue: 2
- Pages: 248-55
- Medium: Print
- Language: English
- Citation (JAMA): Tipton D A, Hamman N R, Dabbous M Kh, et al. Effect of Myrrh Oil on Il-1beta Stimulation of Nf-kappab Activation and Pge(2) Production in Human Gingival Fibroblasts and Epithelial Cells.. Mar 2006;20:248-55
Abstract
Anecdotal and scientific evidence suggest that myrrh oil (MO) has anti-inflammatory properties. Subtoxic MO levels decrease interleukin (IL)-1beta-stimulated production of the inflammatory cytokine IL-6 by human gingival fibroblasts, but not epithelial cells. IL-1beta upregulates IL-6 via PGE(2), and via NF-kappaB, a transcription factor for many inflammatory mediator genes. NF-kappaB is inhibited by sesquiterpene compounds (from plants other than myrrh). This study determined MO effect on IL-1beta-stimulated PGE(2) production and NF-kappaB activation in gingival fibroblasts and epithelial cells. Cells were preincubated with MO, exposed to IL-1beta, cytoplasmic and nuclear fractions were isolated, and activated NF-kappaB was measured using an ELISA-based assay. IL-1beta increased nuclear activated NF-kappaB levels in fibroblasts and epithelial cells [10- and 2.5-fold over controls, respectively (p=0.0001)], and these increases were not significantly affected by MO. PGE(2) was measured in cell supernatants by ELISA, after preincubation with MO and exposure to IL-1beta. MO inhibited IL-1beta-stimulated PGE(2) production by fibroblasts (p=0.001), but not epithelial cells. The data suggest that gingival epithelial cells and fibroblasts may differ in the magnitude of NF-kappaB activation after IL-1beta stimulation, and that MO inhibition of IL-1beta-stimulated IL-6 production in fibroblasts is due in part to inhibition of PGE(2), but not NF-kappaB activation. (Supported by NIDCR DE-0725.).
Mesh Headings (Keywords): Cells, Cultured, Dinoprostone, Epithelial Cells, Fibroblasts, Gingiva, Humans, Interleukin-1, Interleukin-6, Terpenes, Transcription Factor RelA
Check for Full Text / PubMed Unique Identifier (PMID): 16112536
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