Cordycepin alleviates airway hyperreactivity in a murine model of asthma by attenuating the inflammatory process

Int Immunopharmacol. 2015 Jun;26(2):401-8. doi: 10.1016/j.intimp.2015.04.017. Epub 2015 Apr 22.

Abstract

Cordycepin (Cor), which is a naturally occurring nucleoside derivative isolated from Cordyceps militaris, has been shown to exert excellent antiinflammatory activity in a murine model of acute lung injury. Thus, this study aimed to evaluate the antiasthmatic activity of Cor (10, 20, and 40 mg/kg) and to investigate the possible underlying molecular mechanisms. We found that Cor attenuated airway hyperresponsiveness, mucus hypersecretion, and ovalbumin (Ova)-specific immunoglobulin (Ig) E, and alleviated lung inflammation with decreased eosinophils and macrophages in the bronchoalveolar lavage (BAL) fluid. Notably, Cor reduced the upregulation of eotaxin, intercellular cell adhesion molecule-1 (ICAM-1), IL-4, IL-5, and IL-13 in the BAL fluid. Furthermore, Cor markedly blocked p38-MAPK and nuclear factor-kappaB (NF-κB) signalling pathway activation in the Ova-driven asthmatic mice. In conclusion, this study demonstrated that some of the antiasthmatic benefits of Cor attributable to diets and/or tonics may result from reductions in inflammatory processes and that these antiasthmatic properties involve the inhibition of Th2-type responses through the suppression of the p38-MAPK and NF-κB signalling pathways.

Keywords: Allergic inflammation; Cordycepin (Cor); Hyperresponsiveness; Ovalbumin (Ova).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / administration & dosage*
  • Anti-Inflammatory Agents / adverse effects
  • Asthma / drug therapy*
  • Asthma / immunology
  • Bronchial Hyperreactivity / drug therapy*
  • Bronchial Hyperreactivity / immunology
  • Cordyceps / immunology*
  • Cytokines / metabolism
  • Deoxyadenosines / administration & dosage*
  • Deoxyadenosines / adverse effects
  • Eosinophils / drug effects*
  • Eosinophils / immunology
  • Humans
  • Immunoglobulin E / blood
  • Intercellular Adhesion Molecule-1 / genetics
  • Intercellular Adhesion Molecule-1 / metabolism
  • Macrophages / drug effects*
  • Macrophages / immunology
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mucus / metabolism
  • NF-kappa B / metabolism
  • Pneumonia / drug therapy*
  • Pneumonia / immunology
  • Signal Transduction / drug effects
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Anti-Inflammatory Agents
  • Cytokines
  • Deoxyadenosines
  • NF-kappa B
  • Intercellular Adhesion Molecule-1
  • Immunoglobulin E
  • p38 Mitogen-Activated Protein Kinases
  • cordycepin