Cinnamaldehyde derivatives inhibit degranulation and inflammatory mediator production in rat basophilic leukemia cells

Int Immunopharmacol. 2016 Sep:38:342-8. doi: 10.1016/j.intimp.2016.06.018. Epub 2016 Jun 23.

Abstract

Mast cells play a critical role in allergic diseases. Therefore, development of new therapeutic agents that suppresses the activation of mast cells may help prevent or treat allergic diseases. Here, we investigated the anti-allergic effects of 4-chloro-cinnamaldehyde and 4-trifluoro-cinnamaldehyde in RBL-2H3 cells. β-Hexosaminidase assays revealed that degranulation of RBL-2H3 cells was decreased following treatment with 60μM 4-chloro-cinnamaldehyde or 4-trifluoro-cinnamaldehyde. Moreover, quantitative real-time reverse transcription polymerase chain reaction showed that the relative expression levels of tumor necrosis factor-α, interleukin-4, and cyclooxygenase-2 mRNAs were decreased in RBL-2H3 cells treated with 4-chloro-cinnamaldehyde and 4-trifluoro-cinnamaldehyde in a concentration-dependent manner. Additionally, 4-chloro-cinnamaldehyde blocked the phosphorylation of MKKs and MAPKs. These data clearly suggested that 4-chloro-cinnamaldehyde and 4-trifluoro-cinnamaldehyde had inhibitory effects on the inflammatory responses of mast cells and may have potential as novel therapeutic agents for the prevention or treatment of allergic diseases.

Keywords: 4-Chloro-cinnamaldehyde; 4-Trifluoro-cinnamaldehyde; Degranulation; Mitogen-activated protein kinases.

MeSH terms

  • Acrolein / analogs & derivatives*
  • Acrolein / chemistry
  • Acrolein / pharmacology
  • Animals
  • Cell Degranulation / drug effects
  • Cell Line, Tumor
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Gene Expression Regulation / drug effects
  • Humans
  • Hypersensitivity / drug therapy*
  • Hypersensitivity / immunology
  • Inflammation Mediators / metabolism
  • Interleukin-4 / genetics
  • Interleukin-4 / metabolism
  • Mast Cells / drug effects*
  • Mast Cells / physiology
  • Rats
  • Signal Transduction / drug effects
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Inflammation Mediators
  • Tumor Necrosis Factor-alpha
  • Interleukin-4
  • Acrolein
  • Cyclooxygenase 2
  • Extracellular Signal-Regulated MAP Kinases
  • cinnamaldehyde