Anti-inflammatory effects of the cannabidiol derivative dimethylheptyl-cannabidiol - Studies in BV-2 microglia and encephalitogenic T cells

Ana Juknat, Ewa Kozela, Nathali Kaushansky, Raphael Mechoulam, Zvi Vogel*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

33 Scopus citations


Background: Dimethylheptyl-cannabidiol (DMH-CBD), a non-psychoactive, synthetic derivative of the phytocannabinoid cannabidiol (CBD), has been reported to be anti-inflammatory in RAW macrophages. Here, we evaluated the effects of DMH-CBD at the transcriptional level in BV-2 microglial cells as well as on the proliferation of encephalitogenic T cells. Methods: BV-2 cells were pretreated with DMH-CBD, followed by stimulation with the endotoxin lipopolysaccharide (LPS). The expression levels of selected genes involved in stress regulation and inflammation were determined by quantitative real-time PCR. In addition, MOG35-55-reactive T cells (TMOG) were cultured with antigen-presenting cells in the presence of DMH-CBD and MOG35-55 peptide, and cell proliferation was determined by measuring [3H]thymidine incorporation. Results: DMH-CBD treatment downregulated in a dose-dependent manner the mRNA expression of LPS-upregulated pro-inflammatory genes (Il1b, Il6, and Tnf) in BV-2 microglial cells. The expression of these genes was also downregulated by DMH-CBD in unstimulated cells. In parallel, DMH-CBD upregulated the expression of genes related to oxidative stress and glutathione homeostasis such as Trb3, Slc7a11/xCT, Hmox1, Atf4, Chop, and p8 in both stimulated and unstimulated microglial cells. In addition, DMH-CBD dose-dependently inhibited MOG35-55-induced TMOG proliferation. Conclusions: The results show that DMH-CBD has similar anti-inflammatory properties to those of CBD. DMH-CBD downregulates the expression of inflammatory cytokines and protects the microglial cells by inducing an adaptive cellular response against inflammatory stimuli and oxidative injury. In addition, DMH-CBD decreases the proliferation of pathogenic activated TMOG cells.

Original languageAmerican English
Pages (from-to)289-296
Number of pages8
JournalJournal of Basic and Clinical Physiology and Pharmacology
Issue number3
StatePublished - 1 May 2016
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2016 by De Gruyter.


  • T cells
  • anti-inflammation
  • cannabidiol
  • cannabinoids
  • cystine/glutamate transporter
  • dimethylheptyl-cannabidiol
  • gene expression
  • glutathione
  • microglia
  • oxidative stress
  • proliferation


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