The therapeutic efficacy of α-pinene in an experimental mouse model of allergic rhinitis

Int Immunopharmacol. 2014 Nov;23(1):273-82. doi: 10.1016/j.intimp.2014.09.010. Epub 2014 Sep 19.


In the present study, the therapeutic effect and underlying mechanism of α-pinene (α-PN) in the ovalbumin (OVA)-sensitized allergic rhinitis (AR) model were investigated. Our results showed that pretreatment with α-PN caused a decrease in clinical symptoms, including a decrease in the number of nasal, eye, and ear rubs, and spleen weight in the OVA-sensitized mice. The level of interleukin (IL)-4 was decreased on the spleen tissue of α-PN treated mice. Pretreatment with α-PN significantly decreased levels of nasal immunoglobulin E. Protein levels of tumor necrosis factor-α, intercellular adhesion molecule-1, and macrophage inflammatory protein-2 were decreased by the administration of α-PN in the nasal mucosa of the OVA-sensitized mice. The increased numbers of eosinophils and mast cells infiltrating the nasal mucosal tissue of mice with AR were decreased following oral administration of α-PN. Post-treatment with α-PN 1h after OVA challenge also resulted in a significant reduction of clinical symptoms and IgE levels. In addition, the expression and phosphorylation of receptor-interacting protein 2 (RIP2) and IκB kinase (IKK)-β and activation of nuclear factor-κB (NF-κB), and caspase-1 were all increased in the activated human mast cell line, HMC-1 cells, however, increased activations of RIP2, IKK-β, NF-κB, and caspase-1 were inhibited by treatment with α-PN. Taken together, we suggest that α-PN is a promising anti-allergic agent and may be useful in the clinical management of AR.

Keywords: Allergic rhinitis; Inflammation; Mast cells; α-Pinene.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Allergic Agents / therapeutic use*
  • Bicyclic Monoterpenes
  • Caspase 1 / metabolism
  • Cell Line
  • Cell Movement / drug effects
  • Chemokine CXCL2 / genetics
  • Chemokine CXCL2 / metabolism
  • Disease Models, Animal
  • Eosinophils / drug effects*
  • Eosinophils / immunology
  • Female
  • Gene Expression Regulation / drug effects
  • Humans
  • I-kappa B Kinase / metabolism
  • Immunoglobulin E / metabolism
  • Intercellular Adhesion Molecule-1 / genetics
  • Intercellular Adhesion Molecule-1 / metabolism
  • Interleukin-4 / metabolism
  • Mast Cells / drug effects*
  • Mast Cells / immunology
  • Mice, Inbred BALB C
  • Monoterpenes / therapeutic use*
  • NF-kappa B / metabolism
  • Nasal Mucosa / drug effects*
  • Nasal Mucosa / immunology
  • Receptor-Interacting Protein Serine-Threonine Kinase 2 / metabolism
  • Rhinitis, Allergic / drug therapy*
  • Signal Transduction / drug effects
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism


  • Anti-Allergic Agents
  • Bicyclic Monoterpenes
  • Chemokine CXCL2
  • Cxcl2 protein, mouse
  • Icam1 protein, mouse
  • Monoterpenes
  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • Intercellular Adhesion Molecule-1
  • Interleukin-4
  • Immunoglobulin E
  • RIPK2 protein, human
  • Receptor-Interacting Protein Serine-Threonine Kinase 2
  • I-kappa B Kinase
  • Caspase 1
  • alpha-pinene