Inhibitory effects of panduratin A on allergy-related mediator production in rat basophilic leukemia mast cells

Inflammation. 2012 Dec;35(6):1904-15. doi: 10.1007/s10753-012-9513-y.

Abstract

Immediate-type hypersensitivity is characterized by elevated levels of immunoglobulin E (IgE) and activated mast cell plays a crucial role by releasing granule contents, lipid-derived mediators, cytokines, and chemokines. To evaluate the antiallergic effects of panduratin A isolated from Boesenbergia pandurata Roxb., we determined its effects on calcium (Ca(2+)) influx, degranulation, and inflammatory mediators in calcium ionophore A23187 and phorbol 12-myristate 13-acetate (PMA)-stimulated rat basophilic leukemia (RBL-2H3) cells. Panduratin A (20 μM) inhibited secretion of β-hexosaminidase (46.69 ± 9.6 %), histamine (34.32 ± 2.1 %), and Ca(2+) influx (43.84 %). Panduratin A reduced the production of prostaglandin E(2) (PGE(2), 47.58 ± 3.4 %), leukotriene B(4) (LTB(4), 98.15 ± 1.6 %), and the mRNA expression of cyclooxygenase-2, 5-lipoxygenase, interleukin (IL)-4, IL-13, and tumor necrosis factor-α. Furthermore, panduarin A attenuated phosphorylation of Akt, the mitogen-activated protein kinases (MAPK) extracellular signal-regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK) expression. These results indicate that panduratin A might be useful as an agent against immediate-type hypersensitivity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arachidonate 5-Lipoxygenase / genetics
  • Calcimycin / pharmacology
  • Calcium / metabolism
  • Cell Degranulation / drug effects
  • Cell Degranulation / immunology
  • Cell Line, Tumor
  • Chalcones / pharmacology*
  • Cyclooxygenase 2 / genetics
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Histamine / metabolism
  • Histamine Release / drug effects*
  • Histamine Release / immunology
  • Hypersensitivity, Immediate / drug therapy*
  • Immunoglobulin E / immunology
  • Inflammation Mediators
  • Interleukin-13 / genetics
  • Interleukin-4 / genetics
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • Leukemia, Basophilic, Acute / drug therapy*
  • Leukotriene B4 / biosynthesis
  • Mast Cells* / drug effects
  • Mast Cells* / immunology
  • Mast Cells* / metabolism
  • Phosphorylation
  • Plant Extracts / pharmacology
  • Prostaglandins E / biosynthesis
  • Proto-Oncogene Proteins c-akt / metabolism
  • RNA, Messenger / biosynthesis
  • Rats
  • Signal Transduction / immunology
  • Tetradecanoylphorbol Acetate / pharmacology
  • Tumor Necrosis Factor-alpha / genetics
  • Zingiberaceae / metabolism
  • beta-N-Acetylhexosaminidases / drug effects*
  • beta-N-Acetylhexosaminidases / metabolism
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Chalcones
  • Inflammation Mediators
  • Interleukin-13
  • Plant Extracts
  • Prostaglandins E
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Leukotriene B4
  • Interleukin-4
  • panduratin A
  • Immunoglobulin E
  • Calcimycin
  • Histamine
  • Arachidonate 5-Lipoxygenase
  • Cyclooxygenase 2
  • Proto-Oncogene Proteins c-akt
  • Extracellular Signal-Regulated MAP Kinases
  • JNK Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases
  • beta-N-Acetylhexosaminidases
  • Tetradecanoylphorbol Acetate
  • Calcium