Trans-caryophyllene inhibits amyloid β (Aβ) oligomer-induced neuroinflammation in BV-2 microglial cells

Yawei Hu1, Ziling Zeng2, Baojie Wang2

  • 1The Department of Neurosurgery, Affiliated Hospital of Jining Medical University, Jining 272029, Shandong, China.

Insights

Trans-caryophyllene (TC) reduces inflammation in Alzheimer's disease models. This study shows TC protects against amyloid-beta induced neuroinflammation by inhibiting key inflammatory pathways, suggesting its therapeutic potential.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Immunology

Background:

  • Alzheimer's disease (AD) is characterized by amyloid-beta (Aβ) plaques, which trigger neuroinflammation.
  • Microglia activation by Aβ contributes to AD pathogenesis.
  • Trans-caryophyllene (TC), a plant-derived compound, has shown neuroprotective effects, but its role in AD is unclear.

Purpose of the Study:

  • To investigate the therapeutic potential of Trans-caryophyllene (TC) in mitigating amyloid-beta (Aβ)-induced neuroinflammation relevant to Alzheimer's disease (AD).

Main Methods:

  • BV-2 microglial cells were treated with Aβ1-42 and varying concentrations of TC.
  • Assessed lactate dehydrogenase (LDH) release, nitric oxide (NO), prostaglandin E2 (PGE2) production, and pro-inflammatory cytokine secretion.
  • Investigated the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and toll-like receptor 4 (TLR4).
  • Analyzed the NF-κB signaling pathway, including IκBα phosphorylation/degradation, p65 nuclear translocation, and transcriptional activity.

Main Results:

  • TC significantly reduced LDH release in Aβ1-42-treated BV-2 cells.
  • TC pretreatment inhibited NO, PGE2, iNOS, COX-2, and pro-inflammatory cytokine production.
  • TC attenuated Aβ1-42-induced overexpression of TLR4.
  • TC reversed Aβ1-42-induced IκBα degradation, p65 nuclear translocation, and NF-κB activation.

Conclusions:

  • Trans-caryophyllene (TC) demonstrates significant anti-neuroinflammatory effects against amyloid-beta (Aβ) in microglial cells.
  • TC modulates key inflammatory mediators and the NF-κB signaling pathway.
  • These findings highlight TC as a potential therapeutic agent for Alzheimer's disease (AD).

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