Chemical composition and phagocyte immunomodulatory activity of Ferula iliensis essential oils

Gulmira Özek, Igor A. Schepetkin, Gulzhakhan A. Utegenova, Liliya N. Kirpotina, Spencer R. Andrei, Temel Özek, Kemal Hüsnü Can Başer, Karime T. Abidkulova, Svetlana V. Kushnarenko, Andrei I. Khlebnikov, Derek S. Damron, Mark T. Quinn

Research output: Contribution to journalArticlepeer-review

14 Citations (Scopus)


Essential oil extracts from Ferula iliensis have been used traditionally in Kazakhstan for treatment of inflammation and other illnesses. Because little is known about the biologic activity of these essential oils that contributes to their therapeutic properties, we analyzed their chemical composition and evaluated their phagocyte immunomodulatory activity. The main components of the extracted essential oils were (E)-propenyl sec-butyl disulfide (15.7-39.4%) and (Z)-propenyl sec-butyl disulfide (23.4-45.0%). Ferula essential oils stimulated [Ca2+]i mobilization in human neutrophils and activated ROS production in human neutrophils and murine bone marrow phagocytes. Activation of human neutrophil [Ca2+]i flux by Ferula essential oils was dose-dependently inhibited by capsazepine, a TRPV1 channel antagonist, indicating that TRPV1 channels mediate this response. Furthermore, Ferula essential oils stimulated Ca2+ influx in TRPV1 channel-transfected HEK293 cells and desensitized the capsaicin-induced response in these cells. Additional molecular modeling with known TRPV1 channel agonists suggested that the active component is likely to be (Z)-propenyl sec-butyl disulfide. Our results provide a cellular and molecular basis to explain at least part of the beneficial therapeutic properties of FEOs.

Original languageEnglish
Pages (from-to)1361-1371
Number of pages11
JournalJournal of Leukocyte Biology
Issue number6
Publication statusPublished - 1 Jun 2017


  • calcium flux
  • molecular modeling
  • neutrophil
  • reactive oxygen species
  • transient receptor potential vanilloid 1 channel

ASJC Scopus subject areas

  • Immunology
  • Cell Biology

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