β-Caryophyllene ameliorates the Alzheimer-like phenotype in APP/PS1 Mice through CB2 receptor activation and the PPARγ pathway

Pharmacology. 2014;94(1-2):1-12. doi: 10.1159/000362689. Epub 2014 Aug 26.

Abstract

Background/aims: The activation of cannabinoid receptor 2 (CB2) has the beneficial effect of reducing neuroinflammatory response in the treatment of Alzheimer's disease (AD) and is suggested to trigger the peroxisome proliferator-activated receptor-γ (PPARγ) pathway; agonists of both receptors improve AD. Recently, the plant metabolite β-caryophyllene was shown to selectively bind to CB2 receptor and act as a full agonist.

Methods: In this study, we examined the anti-inflammatory effect of β-caryophyllene in a transgenic APP/PS1 AD model and analyzed whether this effect was mediated by CB2 and PPARγ.

Results: β-Caryophyllene, given orally, prevented cognitive impairment in APP/PS1 mice, and this positive cognitive effect was associated with reduced β-amyloid burden in both the hippocampus and the cerebral cortex. Moreover, β-caryophyllene reduced astrogliosis and microglial activation as well as the levels of COX-2 protein and the mRNA levels of the proinflammatory cytokines tumor necrosis factor-α and interleukin-1β in the cerebral cortex. The use of the CB2 antagonist AM630 or the PPARγ antagonist GW9662 significantly reversed the protective effects of β-caryophyllene on APP/PS1 mice.

Conclusion: These results demonstrate that the anti-inflammatory effect of the sesquiterpene β-caryophyllene involves CB2 receptor activation and the PPARγ pathway and suggest β-caryophyllene as an attractive molecule for the development of new drugs with therapeutic potential for the treatment of AD.

MeSH terms

  • Administration, Oral
  • Alzheimer Disease / drug therapy*
  • Alzheimer Disease / physiopathology
  • Amyloid beta-Protein Precursor / genetics
  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / administration & dosage
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
  • Cerebral Cortex / drug effects
  • Cerebral Cortex / metabolism
  • Cognition Disorders / etiology
  • Cognition Disorders / prevention & control
  • Disease Models, Animal
  • Hippocampus / drug effects
  • Hippocampus / metabolism
  • Humans
  • Interleukin-1beta / genetics
  • Male
  • Mice
  • Mice, Transgenic
  • PPAR gamma / metabolism*
  • Polycyclic Sesquiterpenes
  • Presenilin-1 / genetics
  • RNA, Messenger / metabolism
  • Receptor, Cannabinoid, CB2 / agonists
  • Receptor, Cannabinoid, CB2 / metabolism
  • Sesquiterpenes / administration & dosage
  • Sesquiterpenes / pharmacology*
  • Tumor Necrosis Factor-alpha / genetics

Substances

  • APP protein, human
  • Amyloid beta-Protein Precursor
  • Anti-Inflammatory Agents, Non-Steroidal
  • Interleukin-1beta
  • PPAR gamma
  • Polycyclic Sesquiterpenes
  • Presenilin-1
  • RNA, Messenger
  • Receptor, Cannabinoid, CB2
  • Sesquiterpenes
  • Tumor Necrosis Factor-alpha
  • caryophyllene