Protective effects of incensole acetate on cerebral ischemic injury

Arieh Moussaieff, Jin Yu, Hong Zhu, Sebastiano Gattoni-Celli, Esther Shohami, Mark S. Kindy*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

27 Scopus citations


The resin of Boswellia species is a major anti-inflammatory agent that has been used for centuries to treat various conditions including injuries and inflammatory conditions. Incensole acetate (IA), a major constituent of this resin, has been shown to inhibit NF-κB activation and concomitant inflammation, as well as the neurological deficit following head trauma. Here, we show that IA protects against ischemic neuronal damage and reperfusion injury in mice, attenuating the inflammatory nature of ischemic damage. IA given post-ischemia, reduced infarct volumes and improved neurological activities in the mouse model of ischemic injury in a dose dependent fashion. The protection from damage was accompanied by inhibition of TNF-α, IL-1β and TGF-β expression, as well as NF-κB activation following injury. In addition, IA is shown to have a therapeutic window of treatment up to 6 h after ischemic injury. Finally, the protective effects of IA were partially mediated by TRPV3 channels as determined by the TRPV3 deficient mice and channel blocker studies. This study suggests that the anti-inflammatory and neuroprotective activities of IA may serve as a novel therapeutic treatment for ischemic and reperfusion injury, and as a tool in the ongoing research of mechanisms for neurological damage.

Original languageAmerican English
Pages (from-to)89-97
Number of pages9
JournalBrain Research
StatePublished - 14 Mar 2012
Externally publishedYes

Bibliographical note

Funding Information:
We thank Aruna Bhat for her technical support and Eileen McFadden for secretarial support. Supported by grants from the National Institutes of Health ( ES 016774 , MSK), and the Veterans Administration (MSK, SGC) and the National Science Foundation EPSCoR grants (MSK, EPS-0132573 and EPS-0447660 ).


  • Boswellia
  • Cerebral ischemia
  • Incensole acetate
  • Inflammation
  • NF-κB
  • Neuroprotection


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