calcimycin and macelignan

Type I allergy is characterized by the release of granule-associated mediators, lipid-derived substances, cytokines, and chemokines by activated mast cells. To evaluate the anti-allergic effects of macelignan isolated from Myristica fragrans Houtt., we determined its ability to inhibit calcium (Ca(2+)) influx, degranulation, and inflammatory mediator production in RBL-2 H3 cells stimulated with A23187 and phorbol 12-myristate 13-acetate. Macelignan inhibited Ca(2+) influx and the secretion of β-hexosaminidase, histamine, prostaglandin E(2), and leukotriene C(4); decreased mRNA levels of cyclooxygenase-2, 5-lipoxygenase, interleukin-4 (IL-4), IL-13, and tumor necrosis factor-α; and attenuated phosphorylation of Akt and the mitogen-activated protein kinases extracellular signal-regulated kinase, p38, and c-Jun N-terminal kinase. These results indicate the potential of macelignan as a type I allergy treatment.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Arachidonate 5-Lipoxygenase; beta-N-Acetylhexosaminidases; Calcimycin; Calcium; Cell Degranulation; Cell Line, Tumor; Cyclooxygenase 2; Dinoprostone; Extracellular Signal-Regulated MAP Kinases; Histamine Release; Hypersensitivity; Inflammation Mediators; Interleukin-13; Interleukin-4; JNK Mitogen-Activated Protein Kinases; Leukemia, Basophilic, Acute; Leukotriene C4; Lignans; Mast Cells; Myristica; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Plant Extracts; Proto-Oncogene Proteins c-akt; Rats; Tetradecanoylphorbol Acetate; Tumor Necrosis Factor-alpha