Back
Acta Physiologica 2009; Volume 197, Supplement 672
The 60th National Congress of the Italian Physiological Society
9/23/2009-9/25/2009
Siena, Italy
ANTI-INFLAMMATORY EFFECTS OF DEHYDROXYMETHYLEPOXYQUINOMICIN, A NOVEL NF-KB INHIBITOR, IN NORMAL HUMAN KERATINOCYTES NCTC 2544 TREATED WITH IFN- AND HISTAMINE
Abstract number: P31
CARDILE1 V, FRASCA1 G, CAGGIA1 S
1Dip. Scienze Fisiologiche, Univ. di Catania; (Italy)[email protected]
Aim:
A novel NF-kB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ) is a derivative of the antibiotic epoxyquinomicin C from Amycolatopsis sp. and has been found to inhibit tumor necrosis factor (TNF)-a induced activation of NF-kB by suppressing NF-kB nuclear translocation. The present study was set up to determine the effects of DHMEQ at different concentrations of DHMEQ (1, 5 and 10 mg/ml) in normal human keratinocytes NCTC 2544 stimulated or not with 200 U/ml of IFN-g and 10-4 M of histamine.
Methods:
Hydrocortisone (10-5 M) was used as a reference anti-inflammatory drug. After 48 hr each sample was tested for inter-cellular adhesion molecule-1 (ICAM-1), by Western blot analysis, and release of monocyte chemoattractant protein-1 (MCP-1), regulated upon activation normal T-cell expressed and secreted (RANTES) and interleukin-8 (IL-8), through specific sandwich enzyme-linked immunosorbent assay (ELISA). To verify the effect of DHMEQ on cell viability of not stimulated NCTC, the assay of tetrazolium salts metabolization (MTT test) was performed.
Results:
The results demonstrated that DHMEQ is a potent inhibitor of ICAM-1 expression, and MCP-1, RANTES and IL-8 release. MTT assay showed that DHMEQ does not interfere with cell viability. DHMEQ can inhibit the IFN-g and histamine-induced activation of cultured human keratinocytes, which represents an in vitro model of inflamed skin.
Conclusion:
The anti-inflammatory activity of DHMEQ may be exploited by using the drug topically in the skin alone or in combination with subtoxic concentrations of anti-inflammatory drugs in a synergistic manner.
To cite this abstract, please use the following information:
Acta Physiologica 2009; Volume 197, Supplement 672 :P31