Incensole acetate: A novel neuroprotective agent isolated from Boswellia carterii

Arieh Moussaieff, Na'ama A. Shein, Jeanna Tsenter, Savvas Grigoriadis, Constantina Simeonidou, Alexander G. Alexandrovich, Victoria Trembovler, Yinon Ben-Neriah, Michael L. Schmitz, Bernd L. Fiebich, Eduardo Munoz, Raphael Mechoulam, Esther Shohami*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

64 Scopus citations

Abstract

Boswellia resin has been used as a major anti-inflammatory agent and for the healing of wounds for centuries. Incensole acetate (IA), isolated from this resin, was shown to inhibit the activation of nuclear factor-κB, a key transcription factor in the inflammatory response. We now show that IA inhibits the production of inflammatory mediators in an in vitro model system of C6 glioma and human peripheral monocytes. Given the involvement of postinjury inflammation in the pathophysiology and outcome of traumatic brain injury, we examined the effect of IA on the inflammatory process and on the recovery of neurobehavioral and cognitive functions in a mouse model of closed head injury (CHI). In the brains of post-CHI mice, IA reduced glial activation, inhibited the expression of interleukin-1β, and tumor necrosis factor-α mRNAs, and induced cell death in macrophages at the area of trauma. A mild hypothermic effect was also noted. Subsequently, IA inhibited hippocampal neurodegeneration and exerted a beneficial effect on functional outcome after CHI, indicated by reduced neurological severity scores and improved cognitive ability in an object recognition test. This study attributes the anti-inflammatory activity of Boswellia resin to IA and related cembranoid diterpenes and suggests that they may serve as novel neuroprotective agents.

Original languageAmerican English
Pages (from-to)1341-1352
Number of pages12
JournalJournal of Cerebral Blood Flow and Metabolism
Volume28
Issue number7
DOIs
StatePublished - Jul 2008

Keywords

  • Boswellia
  • Cembranoids
  • Incensole acetate
  • Inflammation
  • Neuroprotection
  • Traumatic brain injury

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