Inhibitory effect of quercetin on tryptase and MCP-1 chemokine release, and histidine decarboxylase mRNA transcription by human mast cell-1 cell line
| Autor: | Theoharis C. Theoharides, Duraisamy Kempuraj, Stavros Frydas, Isaia Simeonidou, Pio Conti, Maria Luisa Castellani, Jacopo Vecchiet |
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| Rok vydání: | 2006 |
| Předmět: |
Transcription
Genetic Immunology Tryptase Histidine Decarboxylase Immunoglobulin E Antioxidants Cell Line chemistry.chemical_compound Endocrinology medicine Humans Mast Cells RNA Messenger Interleukin 5 Chemokine CCL2 biology Endocrine and Autonomic Systems Activator (genetics) Reverse Transcriptase Polymerase Chain Reaction Mast cell Blotting Northern Histidine decarboxylase Cell biology Interleukin 33 medicine.anatomical_structure Neurology Biochemistry chemistry biology.protein Quercetin Tryptases Histamine |
| Zdroj: | Neuroimmunomodulation. 13(3) |
| ISSN: | 1021-7401 |
| Popis: | Mast cells are important in reactions of allergic disease and are also involved in a variety of neuroinflammatory diseases. Mast cells can be immunologically activated by IgE through their Fc receptors, as well as by neuropeptides and cytokines to secrete mediators. Here we used a human mast cell-1 (HMC-1) cell line cultured and treated with a physiological activator, anti-IgE, and a nonphysiological activator, calcium ionophore A23187, for tryptase and MCP-1 generation and transcription of histidine decarboxylase. We used quercetin, a potent antioxidant, cytoprotective and anti-inflammatory compound capable of inhibiting histamine and some cytokines released from several cell types, as an inhibitor of immunological and nonimmunological stimulus for mast cells. In this study quercetin inhibits, in a dose-response manner, tryptase and MCP-1. Moreover, using RT-PCR quercetin inhibited the transcription of histidine decarboxylase, the rate-limiting enzyme responsible for the generation of histamine from histidine, and MCP-1. Our data suggest that quercetin is an important and good candidate for reducing the release of pro-inflammatory mast cell mediators activated by physiological and nonphysiological stimulators. |
| Databáze: | OpenAIRE |
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